Re: Insulin related?

Discussion in 'Food and nutrition' started by Andrew B. Chung, MD/PhD, Jan 28, 2006.

  1. kumar wrote:
    > Andrew B. Chung, MD/PhD wrote:
    > > kumar wrote:
    > > > Andrew B. Chung, MD/PhD wrote:
    > > > > kumar wrote:
    > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > kumar wrote:
    > > > > > > > I have following quastions:-
    > > > > > > >
    > > > > > > > 1. Whether enogenous molecules can polymerize in dimers, tetramers,
    > > > > > > > hexamers etc. alfter secretion? If yes, what can be their implications
    > > > > > > > on diabetic patients?
    > > > > > >
    > > > > > > It is not a recognized problem clinically.
    > > > > >
    > > > > > It looks bit odd that long acting exogenous insulin can persist for
    > > > > > long but endogenous not.
    > > > >
    > > > > The exogenous long-acting insulin resides in a different body
    > > > > compartment (subcutaneous).
    > > >
    > > > What will happen when long acting insulin is given intravenously?

    > >
    > > It becomes short acting.
    > >

    > Ok, but can diffused/filtered insulin in other compartments can
    > polymerize and become long acting?


    Exogenous "long-acting" formulations can exist in the subcutaneous
    compartment in the non-physiological form.

    > > > I think insulin in polymeric condition is preserved in low pH or with
    > > > zinc. Higher body pH said to monomerize it. Do slow monomerization or
    > > > long acting is due to lesser blood suply in subcutaneous tissues?

    > >
    > > There is no comparing the subcutaneous body compartment with the
    > > vascular body compartment.
    > >
    > > > What
    > > > is the normal pH of subcutaneous tissues?

    > >
    > > Neutral pH around 7.4
    > >

    > How then long acting insulin become short acting in blood but persist
    > for long in subcutaneous tissues?


    Because of inadequate buffering in the subcutaneous environment, the
    local pH at the injection site will follow the pH of the injection
    solution.

    > > > > > > > 2. Whether exogenous long acting insulin remain in polymer form for
    > > > > > > > long after injecting it? Can it also remain in polymer state for
    > > > > > > > prolonged time(more than as indicated)?
    > > > > > >
    > > > > > > The exact pharmacokinetics will vary from person to person.
    > > > > >
    > > > > > What causes variations in pharmacokinetics of insulin from person to
    > > > > > person?
    > > > >
    > > > > One factor is the amount of subcutaneous body fat.
    > > >
    > > > How amount of subcutaneous body fat causes variations in
    > > > pharmacokinetics of insulin from person to person?

    > >
    > > More body fat means slower release of insulin into the bloodstream.
    > >
    > > > Is it due to as I
    > > > mentioned as above?

    > >
    > > No.
    > >

    > Then how it happens;More body fat means slower release of insulin into
    > the bloodstream?


    More body fat increases the distance from the injection site to the
    vascular compartment.

    > > > > > > > 3. Whether some insulin is not utilized for glucose intake by target
    > > > > > > > cells due to insulin resistance or otherwise? If yes, does it wasted or
    > > > > > > > utilized for other purposes?
    > > > > > >
    > > > > > > The purpose of insulin is to act on target organs as a hormone.
    > > > > >
    > > > > > Yes, but whether all insulin is utilized or not?
    > > > >
    > > > > Hormones are not substrates but rather they are signalling molecules.
    > > > >
    > > > How insulin can perform other actions than causes glucose into the
    > > > cells without its excessive/additional presence?

    > >
    > > Insulin is a signalling molecule that interacts with its receptor,
    > > activating it to phosphorylate other proteins at tyrosines to start a
    > > cascade of post-translation modification leading to enhance glucose
    > > transport into the cell.
    > >

    > Let us say, suppose one million molecules of insulin is reqired to
    > transport 100 million molecules of glucose into the cells in a healthy
    > non-diabetic person and as such all molecules of insulin and all
    > molecules of glucose are metabolized.


    The insulin is not metabolized in the process of interacting with its
    receptors.

    > What will be the appx. ratio in
    > diabetic type2 with insulin resistance patient and whether all
    > molecules of insulin will be metabolized in latter types?


    See above.

    > > > How it it diverted to
    > > > perform other actions without causing hypoglycemia?

    > >
    > > Insulin serves to signal need for glucose uptake at target organs.
    > >

    > Do you want to tell that defficiency of insulin either real or due to
    > its ineffectiveness avtivate body's signals to perform other actions as
    > indicated in link I first provided? In other sense, insulin is not
    > directly required to perform other actions as indicated in link than
    > pursuing glucose entry into cells but its defficiency just trigger
    > other actions. ??


    It is the interaction with its receptor that brings about its effects
    and this interaction is reversible because it does not lead to the
    catabolism of the insulin. This interaction is concentration-dependent
    defined by a binding constant.

    > > > > > > > 4. Whether excess insulin, if present due to excess secretion or
    > > > > > > > stimulated by medicines or injected, will cause above indicated actions
    > > > > > > > in excess or not in insulin resistant patients? It looks if in excess
    > > > > > > > those can be quite harmful?
    > > > > > >
    > > > > > > Excessive insulin can result in hypoglycemic shock.
    > > > > >
    > > > > > Sorry but there are many other actions of insulin.
    > > > >
    > > > > Only when physiological and not excessive.
    > > >
    > > > To perform other functions than to cause glucose into the cells, extra
    > > > insulin is needed to be available.

    > >
    > > No.
    > >
    > > > How such extra insulin stop acting
    > > > for its gulocose related actions and start performing other actions
    > > > without causing hypoglycemia shocks?

    > >
    > > The effects are a function of insulin concentration and not absolute
    > > number of insulin molecules.
    > >
    > > > > > Whether hypoglycemic
    > > > > > shock is pre other actions or after all possible actions of available
    > > > > > insulin?
    > > > >
    > > > > Excessive amounts of insulin will kill before doing anything else.
    > > >
    > > > Instead of this, can't it be polymerize due to its
    > > > concentration(concentration is a reason for its polymerization),
    > > > degrade/denature or become otherwise in-efective esp. in diabetic T2
    > > > people?

    > >
    > > Not in the bloodstream at physiological concentrations.
    > >
    > > >
    > > > > > > > 5. How a insulin resistant patient can get hypoglycemic effect--in view
    > > > > > > > f insulin is not working?
    > > > > > >
    > > > > > > Insulin remains a functional molecule even in insulin resistant
    > > > > > > diabetics.
    > > > > >
    > > > > > Yes but may not completely/efficiently, Can't there be excess insulin
    > > > > > without hypoglycemic shocks due to some disorder?
    > > > >
    > > > > If there is no hypoglycemia, the amount of insulin is not excessive.
    > > >
    > > > Whether normal range of insulin in blood of T2 people can be different
    > > > than non-diabetic people?

    > >
    > > It can be somewhat more.

    >
    > What such more insulin can cause, how it will signal other actions?


    Through its receptors which when activated phosphorylates specific
    intracellular proteins involved in increasing glucose uptake and
    growth.

    Will be available to "glow" and chat about this and other things like
    cardiology, diabetes, cooking and nutrition that interest those
    following this thread here during the next on-line chat (02/02/06) from
    6 to 7 pm EST:

    http://tinyurl.com/cpayh

    For those who are put off by the signature, my advance apologies for
    how the LORD has reshaped me:

    http://tinyurl.com/bgfqt

    Prayerfully in Christ's love,

    Andrew
    http://tinyurl.com/8juld
     
    Tags:


  2. Ken Kubos

    Ken Kubos Guest

    Aaaaah the lord made an obsessive-compulsive (http://www.ocfoundation.org/)
    little man!

    --
    Ken

    "Buddhism elucidates why we are sentient."
    "Karma means that you don't get away with anything."

    "Andrew B. Chung, MD/PhD" <[email protected]> wrote in message
    news:[email protected]
    | kumar wrote:
    |
    | For those who are put off by the signature, my advance apologies for
    | how the LORD has reshaped me:
    |
     
  3. Kumar

    Kumar Guest

    > kumar wrote:
    > > Andrew B. Chung, MD/PhD wrote:
    > > > kumar wrote:
    > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > kumar wrote:
    > > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > > kumar wrote:
    > > > > > > > > I have following quastions:-
    > > > > > > > >
    > > > > > > > > 1. Whether enogenous molecules can polymerize in dimers, tetramers,
    > > > > > > > > hexamers etc. alfter secretion? If yes, what can be their implications
    > > > > > > > > on diabetic patients?
    > > > > > > >
    > > > > > > > It is not a recognized problem clinically.
    > > > > > >
    > > > > > > It looks bit odd that long acting exogenous insulin can persist for
    > > > > > > long but endogenous not.
    > > > > >
    > > > > > The exogenous long-acting insulin resides in a different body
    > > > > > compartment (subcutaneous).
    > > > >
    > > > > What will happen when long acting insulin is given intravenously?
    > > >
    > > > It becomes short acting.
    > > >

    > > Ok, but can diffused/filtered insulin in other compartments can
    > > polymerize and become long acting?

    >
    > Exogenous "long-acting" formulations can exist in the subcutaneous
    > compartment in the non-physiological form.
    >
    > > > > I think insulin in polymeric condition is preserved in low pH or with
    > > > > zinc. Higher body pH said to monomerize it. Do slow monomerization or
    > > > > long acting is due to lesser blood suply in subcutaneous tissues?
    > > >
    > > > There is no comparing the subcutaneous body compartment with the
    > > > vascular body compartment.
    > > >
    > > > > What
    > > > > is the normal pH of subcutaneous tissues?
    > > >
    > > > Neutral pH around 7.4
    > > >

    > > How then long acting insulin become short acting in blood but persist
    > > for long in subcutaneous tissues?

    >
    > Because of inadequate buffering in the subcutaneous environment, the
    > local pH at the injection site will follow the pH of the injection
    > solution.
    >

    I think then, there can be differenciating effects of injecting insulin
    daily due to variations in injecting sites.

    How quick acting insulin injected subcutaneous either individually or
    mixed with long acting affect quickly? Can it move fast due to its
    monomolecular size?
    > > > > > > > > 2. Whether exogenous long acting insulin remain in polymer form for
    > > > > > > > > long after injecting it? Can it also remain in polymer state for
    > > > > > > > > prolonged time(more than as indicated)?
    > > > > > > >
    > > > > > > > The exact pharmacokinetics will vary from person to person.
    > > > > > >
    > > > > > > What causes variations in pharmacokinetics of insulin from person to
    > > > > > > person?
    > > > > >
    > > > > > One factor is the amount of subcutaneous body fat.
    > > > >
    > > > > How amount of subcutaneous body fat causes variations in
    > > > > pharmacokinetics of insulin from person to person?
    > > >
    > > > More body fat means slower release of insulin into the bloodstream.
    > > >
    > > > > Is it due to as I
    > > > > mentioned as above?
    > > >
    > > > No.
    > > >

    > > Then how it happens;More body fat means slower release of insulin into
    > > the bloodstream?

    >
    > More body fat increases the distance from the injection site to the
    > vascular compartment.
    >
    > > > > > > > > 3. Whether some insulin is not utilized for glucose intake by target
    > > > > > > > > cells due to insulin resistance or otherwise? If yes, does it wasted or
    > > > > > > > > utilized for other purposes?
    > > > > > > >
    > > > > > > > The purpose of insulin is to act on target organs as a hormone.
    > > > > > >
    > > > > > > Yes, but whether all insulin is utilized or not?
    > > > > >
    > > > > > Hormones are not substrates but rather they are signalling molecules.
    > > > > >
    > > > > How insulin can perform other actions than causes glucose into the
    > > > > cells without its excessive/additional presence?
    > > >
    > > > Insulin is a signalling molecule that interacts with its receptor,
    > > > activating it to phosphorylate other proteins at tyrosines to start a
    > > > cascade of post-translation modification leading to enhance glucose
    > > > transport into the cell.
    > > >

    > > Let us say, suppose one million molecules of insulin is reqired to
    > > transport 100 million molecules of glucose into the cells in a healthy
    > > non-diabetic person and as such all molecules of insulin and all
    > > molecules of glucose are metabolized.

    >
    > The insulin is not metabolized in the process of interacting with its
    > receptors.
    >

    What will be the fate of such insulin not metabolized in the process of
    interacting with its
    receptors.?
    ?
    > > What will be the appx. ratio in
    > > diabetic type2 with insulin resistance patient and whether all
    > > molecules of insulin will be metabolized in latter types?

    >
    > See above.
    >
    > > > > How it it diverted to
    > > > > perform other actions without causing hypoglycemia?
    > > >
    > > > Insulin serves to signal need for glucose uptake at target organs.
    > > >

    > > Do you want to tell that defficiency of insulin either real or due to
    > > its ineffectiveness avtivate body's signals to perform other actions as
    > > indicated in link I first provided? In other sense, insulin is not
    > > directly required to perform other actions as indicated in link than
    > > pursuing glucose entry into cells but its defficiency just trigger
    > > other actions. ??

    >
    > It is the interaction with its receptor that brings about its effects
    > and this interaction is reversible because it does not lead to the
    > catabolism of the insulin. This interaction is concentration-dependent
    > defined by a binding constant.
    >

    Cells changes regularily,. New cells should be having all receptors
    intact as insulin resistance is not genetically predisposed. Will then
    insulin be normally effective to these new cells?
    > > > > > > > > 4. Whether excess insulin, if present due to excess secretion or
    > > > > > > > > stimulated by medicines or injected, will cause above indicated actions
    > > > > > > > > in excess or not in insulin resistant patients? It looks if in excess
    > > > > > > > > those can be quite harmful?
    > > > > > > >
    > > > > > > > Excessive insulin can result in hypoglycemic shock.
    > > > > > >
    > > > > > > Sorry but there are many other actions of insulin.
    > > > > >
    > > > > > Only when physiological and not excessive.
    > > > >
    > > > > To perform other functions than to cause glucose into the cells, extra
    > > > > insulin is needed to be available.
    > > >
    > > > No.
    > > >
    > > > > How such extra insulin stop acting
    > > > > for its gulocose related actions and start performing other actions
    > > > > without causing hypoglycemia shocks?
    > > >
    > > > The effects are a function of insulin concentration and not absolute
    > > > number of insulin molecules.
    > > >
    > > > > > > Whether hypoglycemic
    > > > > > > shock is pre other actions or after all possible actions of available
    > > > > > > insulin?
    > > > > >
    > > > > > Excessive amounts of insulin will kill before doing anything else.
    > > > >
    > > > > Instead of this, can't it be polymerize due to its
    > > > > concentration(concentration is a reason for its polymerization),
    > > > > degrade/denature or become otherwise in-efective esp. in diabetic T2
    > > > > people?
    > > >
    > > > Not in the bloodstream at physiological concentrations.


    Can/does insulin polymerize at other comprtments than blood? Can
    insulin reverse back from blood into fat tissues polymerize and remain
    there for longer period ? In short does our body has any mechanism by
    which insulin can be stored and persit for longer time?
    > > >
    > > > >
    > > > > > > > > 5. How a insulin resistant patient can get hypoglycemic effect--in view
    > > > > > > > > f insulin is not working?
    > > > > > > >
    > > > > > > > Insulin remains a functional molecule even in insulin resistant
    > > > > > > > diabetics.
    > > > > > >
    > > > > > > Yes but may not completely/efficiently, Can't there be excess insulin
    > > > > > > without hypoglycemic shocks due to some disorder?
    > > > > >
    > > > > > If there is no hypoglycemia, the amount of insulin is not excessive.
    > > > >
    > > > > Whether normal range of insulin in blood of T2 people can be different
    > > > > than non-diabetic people?
    > > >
    > > > It can be somewhat more.

    > >
    > > What such more insulin can cause, how it will signal other actions?

    >
    > Through its receptors which when activated phosphorylates specific
    > intracellular proteins involved in increasing glucose uptake and
    > growth.

    It looks all actions of insulin is primarily glucose related. Ok?

    Thanks you know much more. May be due to both spritual and scientific.
    God bless
     
  4. Kumar wrote:
    > > kumar wrote:
    > > > Andrew B. Chung, MD/PhD wrote:
    > > > > kumar wrote:
    > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > kumar wrote:
    > > > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > > > kumar wrote:
    > > > > > > > > > I have following quastions:-
    > > > > > > > > >
    > > > > > > > > > 1. Whether enogenous molecules can polymerize in dimers, tetramers,
    > > > > > > > > > hexamers etc. alfter secretion? If yes, what can be their implications
    > > > > > > > > > on diabetic patients?
    > > > > > > > >
    > > > > > > > > It is not a recognized problem clinically.
    > > > > > > >
    > > > > > > > It looks bit odd that long acting exogenous insulin can persist for
    > > > > > > > long but endogenous not.
    > > > > > >
    > > > > > > The exogenous long-acting insulin resides in a different body
    > > > > > > compartment (subcutaneous).
    > > > > >
    > > > > > What will happen when long acting insulin is given intravenously?
    > > > >
    > > > > It becomes short acting.
    > > > >
    > > > Ok, but can diffused/filtered insulin in other compartments can
    > > > polymerize and become long acting?

    > >
    > > Exogenous "long-acting" formulations can exist in the subcutaneous
    > > compartment in the non-physiological form.
    > >
    > > > > > I think insulin in polymeric condition is preserved in low pH or with
    > > > > > zinc. Higher body pH said to monomerize it. Do slow monomerization or
    > > > > > long acting is due to lesser blood suply in subcutaneous tissues?
    > > > >
    > > > > There is no comparing the subcutaneous body compartment with the
    > > > > vascular body compartment.
    > > > >
    > > > > > What
    > > > > > is the normal pH of subcutaneous tissues?
    > > > >
    > > > > Neutral pH around 7.4
    > > > >
    > > > How then long acting insulin become short acting in blood but persist
    > > > for long in subcutaneous tissues?

    > >
    > > Because of inadequate buffering in the subcutaneous environment, the
    > > local pH at the injection site will follow the pH of the injection
    > > solution.
    > >

    > I think then, there can be differenciating effects of injecting insulin
    > daily due to variations in injecting sites.


    In practice, we don't see it probably because the amount of food that
    people eat varies widely.

    > How quick acting insulin injected subcutaneous either individually or
    > mixed with long acting affect quickly? Can it move fast due to its
    > monomolecular size?


    Yes.

    > > > > > > > > > 2. Whether exogenous long acting insulin remain in polymer form for
    > > > > > > > > > long after injecting it? Can it also remain in polymer state for
    > > > > > > > > > prolonged time(more than as indicated)?
    > > > > > > > >
    > > > > > > > > The exact pharmacokinetics will vary from person to person.
    > > > > > > >
    > > > > > > > What causes variations in pharmacokinetics of insulin from person to
    > > > > > > > person?
    > > > > > >
    > > > > > > One factor is the amount of subcutaneous body fat.
    > > > > >
    > > > > > How amount of subcutaneous body fat causes variations in
    > > > > > pharmacokinetics of insulin from person to person?
    > > > >
    > > > > More body fat means slower release of insulin into the bloodstream.
    > > > >
    > > > > > Is it due to as I
    > > > > > mentioned as above?
    > > > >
    > > > > No.
    > > > >
    > > > Then how it happens;More body fat means slower release of insulin into
    > > > the bloodstream?

    > >
    > > More body fat increases the distance from the injection site to the
    > > vascular compartment.
    > >
    > > > > > > > > > 3. Whether some insulin is not utilized for glucose intake by target
    > > > > > > > > > cells due to insulin resistance or otherwise? If yes, does it wasted or
    > > > > > > > > > utilized for other purposes?
    > > > > > > > >
    > > > > > > > > The purpose of insulin is to act on target organs as a hormone.
    > > > > > > >
    > > > > > > > Yes, but whether all insulin is utilized or not?
    > > > > > >
    > > > > > > Hormones are not substrates but rather they are signalling molecules.
    > > > > > >
    > > > > > How insulin can perform other actions than causes glucose into the
    > > > > > cells without its excessive/additional presence?
    > > > >
    > > > > Insulin is a signalling molecule that interacts with its receptor,
    > > > > activating it to phosphorylate other proteins at tyrosines to start a
    > > > > cascade of post-translation modification leading to enhance glucose
    > > > > transport into the cell.
    > > > >
    > > > Let us say, suppose one million molecules of insulin is reqired to
    > > > transport 100 million molecules of glucose into the cells in a healthy
    > > > non-diabetic person and as such all molecules of insulin and all
    > > > molecules of glucose are metabolized.

    > >
    > > The insulin is not metabolized in the process of interacting with its
    > > receptors.
    > >

    > What will be the fate of such insulin not metabolized in the process of
    > interacting with its
    > receptors.?


    It has additional opportunities for intermolecular interactions.

    > > > What will be the appx. ratio in
    > > > diabetic type2 with insulin resistance patient and whether all
    > > > molecules of insulin will be metabolized in latter types?

    > >
    > > See above.
    > >
    > > > > > How it it diverted to
    > > > > > perform other actions without causing hypoglycemia?
    > > > >
    > > > > Insulin serves to signal need for glucose uptake at target organs.
    > > > >
    > > > Do you want to tell that defficiency of insulin either real or due to
    > > > its ineffectiveness avtivate body's signals to perform other actions as
    > > > indicated in link I first provided? In other sense, insulin is not
    > > > directly required to perform other actions as indicated in link than
    > > > pursuing glucose entry into cells but its defficiency just trigger
    > > > other actions. ??

    > >
    > > It is the interaction with its receptor that brings about its effects
    > > and this interaction is reversible because it does not lead to the
    > > catabolism of the insulin. This interaction is concentration-dependent
    > > defined by a binding constant.
    > >

    > Cells changes regularily,.


    The receptors don't,

    > New cells should be having all receptors
    > intact as insulin resistance is not genetically predisposed.


    Actually, there is a genetic predisposition toward developing insulin
    resistance.

    > Will then
    > insulin be normally effective to these new cells?


    Not in the setting of metabolic syndrome (MetS).

    > > > > > > > > > 4. Whether excess insulin, if present due to excess secretion or
    > > > > > > > > > stimulated by medicines or injected, will cause above indicated actions
    > > > > > > > > > in excess or not in insulin resistant patients? It looks if in excess
    > > > > > > > > > those can be quite harmful?
    > > > > > > > >
    > > > > > > > > Excessive insulin can result in hypoglycemic shock.
    > > > > > > >
    > > > > > > > Sorry but there are many other actions of insulin.
    > > > > > >
    > > > > > > Only when physiological and not excessive.
    > > > > >
    > > > > > To perform other functions than to cause glucose into the cells, extra
    > > > > > insulin is needed to be available.
    > > > >
    > > > > No.
    > > > >
    > > > > > How such extra insulin stop acting
    > > > > > for its gulocose related actions and start performing other actions
    > > > > > without causing hypoglycemia shocks?
    > > > >
    > > > > The effects are a function of insulin concentration and not absolute
    > > > > number of insulin molecules.
    > > > >
    > > > > > > > Whether hypoglycemic
    > > > > > > > shock is pre other actions or after all possible actions of available
    > > > > > > > insulin?
    > > > > > >
    > > > > > > Excessive amounts of insulin will kill before doing anything else.
    > > > > >
    > > > > > Instead of this, can't it be polymerize due to its
    > > > > > concentration(concentration is a reason for its polymerization),
    > > > > > degrade/denature or become otherwise in-efective esp. in diabetic T2
    > > > > > people?
    > > > >
    > > > > Not in the bloodstream at physiological concentrations.

    >
    > Can/does insulin polymerize at other comprtments than blood?


    Hydrostatic and electrostatic interactions do not involve the formation
    of covalent bonds necessary for polymerization.

    > Can
    > insulin reverse back from blood into fat tissues polymerize and remain
    > there for longer period ?


    No.

    > In short does our body has any mechanism by
    > which insulin can be stored and persit for longer time?


    No. If it did, insulin would lose its ability to signal.

    > > > >
    > > > > >
    > > > > > > > > > 5. How a insulin resistant patient can get hypoglycemic effect--in view
    > > > > > > > > > f insulin is not working?
    > > > > > > > >
    > > > > > > > > Insulin remains a functional molecule even in insulin resistant
    > > > > > > > > diabetics.
    > > > > > > >
    > > > > > > > Yes but may not completely/efficiently, Can't there be excess insulin
    > > > > > > > without hypoglycemic shocks due to some disorder?
    > > > > > >
    > > > > > > If there is no hypoglycemia, the amount of insulin is not excessive.
    > > > > >
    > > > > > Whether normal range of insulin in blood of T2 people can be different
    > > > > > than non-diabetic people?
    > > > >
    > > > > It can be somewhat more.
    > > >
    > > > What such more insulin can cause, how it will signal other actions?

    > >
    > > Through its receptors which when activated phosphorylates specific
    > > intracellular proteins involved in increasing glucose uptake and
    > > growth.

    > It looks all actions of insulin is primarily glucose related. Ok?


    It also promotes growth.

    > Thanks you know much more. May be due to both spritual and scientific.


    It is all due to the LORD, Whom I love with all my being :))

    > God bless


    Thank you for your kind thoughts.

    Will be available to "glow" and chat about this and other things like
    cardiology, diabetes, cooking and nutrition that interest those
    following this thread here during the next on-line chat (02/02/06) from
    6 to 7 pm EST:

    http://tinyurl.com/cpayh

    For those who are put off by the signature, my advance apologies for
    how the LORD has reshaped me:

    http://tinyurl.com/bgfqt

    Prayerfully in Christ's love,

    Andrew
    http://tinyurl.com/8juld
     
  5. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > > kumar wrote:
    > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > kumar wrote:
    > > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > > kumar wrote:
    > > > > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > > > > kumar wrote:
    > > > > > > > > > > I have following quastions:-
    > > > > > > > > > >
    > > > > > > > > > > 1. Whether enogenous molecules can polymerize in dimers, tetramers,
    > > > > > > > > > > hexamers etc. alfter secretion? If yes, what can be their implications
    > > > > > > > > > > on diabetic patients?
    > > > > > > > > >
    > > > > > > > > > It is not a recognized problem clinically.
    > > > > > > > >
    > > > > > > > > It looks bit odd that long acting exogenous insulin can persist for
    > > > > > > > > long but endogenous not.
    > > > > > > >
    > > > > > > > The exogenous long-acting insulin resides in a different body
    > > > > > > > compartment (subcutaneous).
    > > > > > >
    > > > > > > What will happen when long acting insulin is given intravenously?
    > > > > >
    > > > > > It becomes short acting.
    > > > > >
    > > > > Ok, but can diffused/filtered insulin in other compartments can
    > > > > polymerize and become long acting?
    > > >
    > > > Exogenous "long-acting" formulations can exist in the subcutaneous
    > > > compartment in the non-physiological form.
    > > >
    > > > > > > I think insulin in polymeric condition is preserved in low pH or with
    > > > > > > zinc. Higher body pH said to monomerize it. Do slow monomerization or
    > > > > > > long acting is due to lesser blood suply in subcutaneous tissues?
    > > > > >
    > > > > > There is no comparing the subcutaneous body compartment with the
    > > > > > vascular body compartment.
    > > > > >
    > > > > > > What
    > > > > > > is the normal pH of subcutaneous tissues?
    > > > > >
    > > > > > Neutral pH around 7.4
    > > > > >
    > > > > How then long acting insulin become short acting in blood but persist
    > > > > for long in subcutaneous tissues?
    > > >
    > > > Because of inadequate buffering in the subcutaneous environment, the
    > > > local pH at the injection site will follow the pH of the injection
    > > > solution.
    > > >

    > > I think then, there can be differenciating effects of injecting insulin
    > > daily due to variations in injecting sites.

    >
    > In practice, we don't see it probably because the amount of food that
    > people eat varies widely.
    >

    Previously when syringe with long needle was common for injecting
    insulin, insulin was better controlled. Now pen nd short needle is
    common. Can there be some variations in effect by injected insulin
    (esp. long cting) due to size of needle in view of these discussions?
    > > How quick acting insulin injected subcutaneous either individually or
    > > mixed with long acting affect quickly? Can it move fast due to its
    > > monomolecular size?

    >
    > Yes.
    >

    Is there any other resistance in transporting injected insulin to
    vascular compartment?

    > > > > > > > > > > 2. Whether exogenous long acting insulin remain in polymer form for
    > > > > > > > > > > long after injecting it? Can it also remain in polymer state for
    > > > > > > > > > > prolonged time(more than as indicated)?
    > > > > > > > > >
    > > > > > > > > > The exact pharmacokinetics will vary from person to person.
    > > > > > > > >
    > > > > > > > > What causes variations in pharmacokinetics of insulin from person to
    > > > > > > > > person?
    > > > > > > >
    > > > > > > > One factor is the amount of subcutaneous body fat.
    > > > > > >
    > > > > > > How amount of subcutaneous body fat causes variations in
    > > > > > > pharmacokinetics of insulin from person to person?
    > > > > >
    > > > > > More body fat means slower release of insulin into the bloodstream.
    > > > > >
    > > > > > > Is it due to as I
    > > > > > > mentioned as above?
    > > > > >
    > > > > > No.
    > > > > >
    > > > > Then how it happens;More body fat means slower release of insulin into
    > > > > the bloodstream?
    > > >
    > > > More body fat increases the distance from the injection site to the
    > > > vascular compartment.
    > > >
    > > > > > > > > > > 3. Whether some insulin is not utilized for glucose intake by target
    > > > > > > > > > > cells due to insulin resistance or otherwise? If yes, does it wasted or
    > > > > > > > > > > utilized for other purposes?
    > > > > > > > > >
    > > > > > > > > > The purpose of insulin is to act on target organs as a hormone.
    > > > > > > > >
    > > > > > > > > Yes, but whether all insulin is utilized or not?
    > > > > > > >
    > > > > > > > Hormones are not substrates but rather they are signalling molecules.
    > > > > > > >
    > > > > > > How insulin can perform other actions than causes glucose into the
    > > > > > > cells without its excessive/additional presence?
    > > > > >
    > > > > > Insulin is a signalling molecule that interacts with its receptor,
    > > > > > activating it to phosphorylate other proteins at tyrosines to start a
    > > > > > cascade of post-translation modification leading to enhance glucose
    > > > > > transport into the cell.
    > > > > >
    > > > > Let us say, suppose one million molecules of insulin is reqired to
    > > > > transport 100 million molecules of glucose into the cells in a healthy
    > > > > non-diabetic person and as such all molecules of insulin and all
    > > > > molecules of glucose are metabolized.
    > > >
    > > > The insulin is not metabolized in the process of interacting with its
    > > > receptors.
    > > >

    > > What will be the fate of such insulin not metabolized in the process of
    > > interacting with its
    > > receptors.?

    >
    > It has additional opportunities for intermolecular interactions.
    >

    What are these intermolecular interactions?
    > > > > What will be the appx. ratio in
    > > > > diabetic type2 with insulin resistance patient and whether all
    > > > > molecules of insulin will be metabolized in latter types?
    > > >
    > > > See above.
    > > >
    > > > > > > How it it diverted to
    > > > > > > perform other actions without causing hypoglycemia?
    > > > > >
    > > > > > Insulin serves to signal need for glucose uptake at target organs.
    > > > > >
    > > > > Do you want to tell that defficiency of insulin either real or due to
    > > > > its ineffectiveness avtivate body's signals to perform other actions as
    > > > > indicated in link I first provided? In other sense, insulin is not
    > > > > directly required to perform other actions as indicated in link than
    > > > > pursuing glucose entry into cells but its defficiency just trigger
    > > > > other actions. ??
    > > >
    > > > It is the interaction with its receptor that brings about its effects
    > > > and this interaction is reversible because it does not lead to the
    > > > catabolism of the insulin. This interaction is concentration-dependent
    > > > defined by a binding constant.
    > > >

    > > Cells changes regularily,.

    >
    > The receptors don't,
    >
    > > New cells should be having all receptors
    > > intact as insulin resistance is not genetically predisposed.

    >
    > Actually, there is a genetic predisposition toward developing insulin
    > resistance.
    >

    How then it is reversible by correcting obesity esp.in diabetics who
    have not yet start taking insulin injections?
    > > Will then
    > > insulin be normally effective to these new cells?

    >
    > Not in the setting of metabolic syndrome (MetS).
    >
    > > > > > > > > > > 4. Whether excess insulin, if present due to excess secretion or
    > > > > > > > > > > stimulated by medicines or injected, will cause above indicated actions
    > > > > > > > > > > in excess or not in insulin resistant patients? It looks if in excess
    > > > > > > > > > > those can be quite harmful?
    > > > > > > > > >
    > > > > > > > > > Excessive insulin can result in hypoglycemic shock.
    > > > > > > > >
    > > > > > > > > Sorry but there are many other actions of insulin.
    > > > > > > >
    > > > > > > > Only when physiological and not excessive.
    > > > > > >
    > > > > > > To perform other functions than to cause glucose into the cells, extra
    > > > > > > insulin is needed to be available.
    > > > > >
    > > > > > No.
    > > > > >
    > > > > > > How such extra insulin stop acting
    > > > > > > for its gulocose related actions and start performing other actions
    > > > > > > without causing hypoglycemia shocks?
    > > > > >
    > > > > > The effects are a function of insulin concentration and not absolute
    > > > > > number of insulin molecules.
    > > > > >
    > > > > > > > > Whether hypoglycemic
    > > > > > > > > shock is pre other actions or after all possible actions of available
    > > > > > > > > insulin?
    > > > > > > >
    > > > > > > > Excessive amounts of insulin will kill before doing anything else.
    > > > > > >
    > > > > > > Instead of this, can't it be polymerize due to its
    > > > > > > concentration(concentration is a reason for its polymerization),
    > > > > > > degrade/denature or become otherwise in-efective esp. in diabetic T2
    > > > > > > people?
    > > > > >
    > > > > > Not in the bloodstream at physiological concentrations.

    > >
    > > Can/does insulin polymerize at other comprtments than blood?

    >
    > Hydrostatic and electrostatic interactions do not involve the formation
    > of covalent bonds necessary for polymerization.
    >

    Sorry but I think, It is intermolecular association attached by
    intermolecular forces necessary for polymerization not by covalent
    bonding.
    > > Can
    > > insulin reverse back from blood into fat tissues polymerize and remain
    > > there for longer period ?

    >
    > No.
    >
    > > In short does our body has any mechanism by
    > > which insulin can be stored and persit for longer time?

    >
    > No. If it did, insulin would lose its ability to signal.
    >

    Yes, but on getting diabeteswith IR, it looks alike as insulin is
    working lesser.
    > > > > >
    > > > > > >
    > > > > > > > > > > 5. How a insulin resistant patient can get hypoglycemic effect--in view
    > > > > > > > > > > f insulin is not working?
    > > > > > > > > >
    > > > > > > > > > Insulin remains a functional molecule even in insulin resistant
    > > > > > > > > > diabetics.
    > > > > > > > >
    > > > > > > > > Yes but may not completely/efficiently, Can't there be excess insulin
    > > > > > > > > without hypoglycemic shocks due to some disorder?
    > > > > > > >
    > > > > > > > If there is no hypoglycemia, the amount of insulin is not excessive.
    > > > > > >
    > > > > > > Whether normal range of insulin in blood of T2 people can be different
    > > > > > > than non-diabetic people?
    > > > > >
    > > > > > It can be somewhat more.
    > > > >
    > > > > What such more insulin can cause, how it will signal other actions?
    > > >
    > > > Through its receptors which when activated phosphorylates specific
    > > > intracellular proteins involved in increasing glucose uptake and
    > > > growth.

    > > It looks all actions of insulin is primarily glucose related. Ok?

    >
    > It also promotes growth.
    >

    How?
    > > Thanks you know much more. May be due to both spritual and scientific.

    >
    > It is all due to the LORD, Whom I love with all my being :))
    >
    > > God bless

    >
    > Thank you for your kind thoughts.
     
  6. Kumar wrote:
    > Andrew B. Chung, MD/PhD wrote:
    > > Kumar wrote:
    > > > > kumar wrote:
    > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > kumar wrote:
    > > > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > > > kumar wrote:
    > > > > > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > > > > > kumar wrote:
    > > > > > > > > > > > I have following quastions:-
    > > > > > > > > > > >
    > > > > > > > > > > > 1. Whether enogenous molecules can polymerize in dimers, tetramers,
    > > > > > > > > > > > hexamers etc. alfter secretion? If yes, what can be their implications
    > > > > > > > > > > > on diabetic patients?
    > > > > > > > > > >
    > > > > > > > > > > It is not a recognized problem clinically.
    > > > > > > > > >
    > > > > > > > > > It looks bit odd that long acting exogenous insulin can persist for
    > > > > > > > > > long but endogenous not.
    > > > > > > > >
    > > > > > > > > The exogenous long-acting insulin resides in a different body
    > > > > > > > > compartment (subcutaneous).
    > > > > > > >
    > > > > > > > What will happen when long acting insulin is given intravenously?
    > > > > > >
    > > > > > > It becomes short acting.
    > > > > > >
    > > > > > Ok, but can diffused/filtered insulin in other compartments can
    > > > > > polymerize and become long acting?
    > > > >
    > > > > Exogenous "long-acting" formulations can exist in the subcutaneous
    > > > > compartment in the non-physiological form.
    > > > >
    > > > > > > > I think insulin in polymeric condition is preserved in low pH or with
    > > > > > > > zinc. Higher body pH said to monomerize it. Do slow monomerization or
    > > > > > > > long acting is due to lesser blood suply in subcutaneous tissues?
    > > > > > >
    > > > > > > There is no comparing the subcutaneous body compartment with the
    > > > > > > vascular body compartment.
    > > > > > >
    > > > > > > > What
    > > > > > > > is the normal pH of subcutaneous tissues?
    > > > > > >
    > > > > > > Neutral pH around 7.4
    > > > > > >
    > > > > > How then long acting insulin become short acting in blood but persist
    > > > > > for long in subcutaneous tissues?
    > > > >
    > > > > Because of inadequate buffering in the subcutaneous environment, the
    > > > > local pH at the injection site will follow the pH of the injection
    > > > > solution.
    > > > >
    > > > I think then, there can be differenciating effects of injecting insulin
    > > > daily due to variations in injecting sites.

    > >
    > > In practice, we don't see it probably because the amount of food that
    > > people eat varies widely.
    > >

    > Previously when syringe with long needle was common for injecting
    > insulin, insulin was better controlled. Now pen nd short needle is
    > common. Can there be some variations in effect by injected insulin
    > (esp. long cting) due to size of needle in view of these discussions?


    I have not noticed it.

    > > > How quick acting insulin injected subcutaneous either individually or
    > > > mixed with long acting affect quickly? Can it move fast due to its
    > > > monomolecular size?

    > >
    > > Yes.
    > >

    > Is there any other resistance in transporting injected insulin to
    > vascular compartment?


    No.

    > > > > > > > > > > > 2. Whether exogenous long acting insulin remain in polymer form for
    > > > > > > > > > > > long after injecting it? Can it also remain in polymer state for
    > > > > > > > > > > > prolonged time(more than as indicated)?
    > > > > > > > > > >
    > > > > > > > > > > The exact pharmacokinetics will vary from person to person.
    > > > > > > > > >
    > > > > > > > > > What causes variations in pharmacokinetics of insulin from person to
    > > > > > > > > > person?
    > > > > > > > >
    > > > > > > > > One factor is the amount of subcutaneous body fat.
    > > > > > > >
    > > > > > > > How amount of subcutaneous body fat causes variations in
    > > > > > > > pharmacokinetics of insulin from person to person?
    > > > > > >
    > > > > > > More body fat means slower release of insulin into the bloodstream.
    > > > > > >
    > > > > > > > Is it due to as I
    > > > > > > > mentioned as above?
    > > > > > >
    > > > > > > No.
    > > > > > >
    > > > > > Then how it happens;More body fat means slower release of insulin into
    > > > > > the bloodstream?
    > > > >
    > > > > More body fat increases the distance from the injection site to the
    > > > > vascular compartment.
    > > > >
    > > > > > > > > > > > 3. Whether some insulin is not utilized for glucose intake by target
    > > > > > > > > > > > cells due to insulin resistance or otherwise? If yes, does it wasted or
    > > > > > > > > > > > utilized for other purposes?
    > > > > > > > > > >
    > > > > > > > > > > The purpose of insulin is to act on target organs as a hormone.
    > > > > > > > > >
    > > > > > > > > > Yes, but whether all insulin is utilized or not?
    > > > > > > > >
    > > > > > > > > Hormones are not substrates but rather they are signalling molecules.
    > > > > > > > >
    > > > > > > > How insulin can perform other actions than causes glucose into the
    > > > > > > > cells without its excessive/additional presence?
    > > > > > >
    > > > > > > Insulin is a signalling molecule that interacts with its receptor,
    > > > > > > activating it to phosphorylate other proteins at tyrosines to start a
    > > > > > > cascade of post-translation modification leading to enhance glucose
    > > > > > > transport into the cell.
    > > > > > >
    > > > > > Let us say, suppose one million molecules of insulin is reqired to
    > > > > > transport 100 million molecules of glucose into the cells in a healthy
    > > > > > non-diabetic person and as such all molecules of insulin and all
    > > > > > molecules of glucose are metabolized.
    > > > >
    > > > > The insulin is not metabolized in the process of interacting with its
    > > > > receptors.
    > > > >
    > > > What will be the fate of such insulin not metabolized in the process of
    > > > interacting with its
    > > > receptors.?

    > >
    > > It has additional opportunities for intermolecular interactions.
    > >

    > What are these intermolecular interactions?


    Receptor binding.

    > > > > > What will be the appx. ratio in
    > > > > > diabetic type2 with insulin resistance patient and whether all
    > > > > > molecules of insulin will be metabolized in latter types?
    > > > >
    > > > > See above.
    > > > >
    > > > > > > > How it it diverted to
    > > > > > > > perform other actions without causing hypoglycemia?
    > > > > > >
    > > > > > > Insulin serves to signal need for glucose uptake at target organs.
    > > > > > >
    > > > > > Do you want to tell that defficiency of insulin either real or due to
    > > > > > its ineffectiveness avtivate body's signals to perform other actions as
    > > > > > indicated in link I first provided? In other sense, insulin is not
    > > > > > directly required to perform other actions as indicated in link than
    > > > > > pursuing glucose entry into cells but its defficiency just trigger
    > > > > > other actions. ??
    > > > >
    > > > > It is the interaction with its receptor that brings about its effects
    > > > > and this interaction is reversible because it does not lead to the
    > > > > catabolism of the insulin. This interaction is concentration-dependent
    > > > > defined by a binding constant.
    > > > >
    > > > Cells changes regularily,.

    > >
    > > The receptors don't,
    > >
    > > > New cells should be having all receptors
    > > > intact as insulin resistance is not genetically predisposed.

    > >
    > > Actually, there is a genetic predisposition toward developing insulin
    > > resistance.
    > >

    > How then it is reversible by correcting obesity esp.in diabetics who
    > have not yet start taking insulin injections?


    By decreasing levels of inflammatory cytokines which are produced by
    visceral adipocytes.

    > > > Will then
    > > > insulin be normally effective to these new cells?

    > >
    > > Not in the setting of metabolic syndrome (MetS).
    > >
    > > > > > > > > > > > 4. Whether excess insulin, if present due to excess secretion or
    > > > > > > > > > > > stimulated by medicines or injected, will cause above indicated actions
    > > > > > > > > > > > in excess or not in insulin resistant patients? It looks if in excess
    > > > > > > > > > > > those can be quite harmful?
    > > > > > > > > > >
    > > > > > > > > > > Excessive insulin can result in hypoglycemic shock.
    > > > > > > > > >
    > > > > > > > > > Sorry but there are many other actions of insulin.
    > > > > > > > >
    > > > > > > > > Only when physiological and not excessive.
    > > > > > > >
    > > > > > > > To perform other functions than to cause glucose into the cells, extra
    > > > > > > > insulin is needed to be available.
    > > > > > >
    > > > > > > No.
    > > > > > >
    > > > > > > > How such extra insulin stop acting
    > > > > > > > for its gulocose related actions and start performing other actions
    > > > > > > > without causing hypoglycemia shocks?
    > > > > > >
    > > > > > > The effects are a function of insulin concentration and not absolute
    > > > > > > number of insulin molecules.
    > > > > > >
    > > > > > > > > > Whether hypoglycemic
    > > > > > > > > > shock is pre other actions or after all possible actions of available
    > > > > > > > > > insulin?
    > > > > > > > >
    > > > > > > > > Excessive amounts of insulin will kill before doing anything else.
    > > > > > > >
    > > > > > > > Instead of this, can't it be polymerize due to its
    > > > > > > > concentration(concentration is a reason for its polymerization),
    > > > > > > > degrade/denature or become otherwise in-efective esp. in diabetic T2
    > > > > > > > people?
    > > > > > >
    > > > > > > Not in the bloodstream at physiological concentrations.
    > > >
    > > > Can/does insulin polymerize at other comprtments than blood?

    > >
    > > Hydrostatic and electrostatic interactions do not involve the formation
    > > of covalent bonds necessary for polymerization.
    > >

    > Sorry but I think, It is intermolecular association attached by
    > intermolecular forces necessary for polymerization not by covalent
    > bonding.


    The term polymerization, by definition, involves the formation of
    covalent bonds.

    > > > Can
    > > > insulin reverse back from blood into fat tissues polymerize and remain
    > > > there for longer period ?

    > >
    > > No.
    > >
    > > > In short does our body has any mechanism by
    > > > which insulin can be stored and persit for longer time?

    > >
    > > No. If it did, insulin would lose its ability to signal.
    > >

    > Yes, but on getting diabeteswith IR, it looks alike as insulin is
    > working lesser.


    It still works as a signal even if less effectively.

    > > > > > >
    > > > > > > >
    > > > > > > > > > > > 5. How a insulin resistant patient can get hypoglycemic effect--in view
    > > > > > > > > > > > f insulin is not working?
    > > > > > > > > > >
    > > > > > > > > > > Insulin remains a functional molecule even in insulin resistant
    > > > > > > > > > > diabetics.
    > > > > > > > > >
    > > > > > > > > > Yes but may not completely/efficiently, Can't there be excess insulin
    > > > > > > > > > without hypoglycemic shocks due to some disorder?
    > > > > > > > >
    > > > > > > > > If there is no hypoglycemia, the amount of insulin is not excessive.
    > > > > > > >
    > > > > > > > Whether normal range of insulin in blood of T2 people can be different
    > > > > > > > than non-diabetic people?
    > > > > > >
    > > > > > > It can be somewhat more.
    > > > > >
    > > > > > What such more insulin can cause, how it will signal other actions?
    > > > >
    > > > > Through its receptors which when activated phosphorylates specific
    > > > > intracellular proteins involved in increasing glucose uptake and
    > > > > growth.
    > > > It looks all actions of insulin is primarily glucose related. Ok?

    > >
    > > It also promotes growth.
    > >

    > How?


    Through receptor-mediated post-translational modification (tyrosine
    phosporylation) of intracellular proteins involved in cellular growth.

    Will be available to "glow" and chat about this and other things like
    cardiology, diabetes, cooking and nutrition that interest those
    following this thread here during the next on-line chat (02/02/06) from
    6 to 7 pm EST:

    http://tinyurl.com/cpayh

    For those who are put off by the signature, my advance apologies for
    how the LORD has reshaped me:

    http://tinyurl.com/bgfqt

    Prayerfully in Christ's love,

    Andrew
    http://tinyurl.com/8juld
     
  7. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > Is there any other resistance in transporting injected insulin to
    > > vascular compartment?

    >
    > No.
    >


    Can insulin molecules in blood or at other compartment be aggregated or
    associated by intermolecular forces without polymerization? If yes, can
    this condition exist for long?

    > > What are these intermolecular interactions?

    >
    > Receptor binding.
    >

    Good thanks.
    > > > Actually, there is a genetic predisposition toward developing insulin
    > > > resistance.
    > > >

    > > How then it is reversible by correcting obesity esp.in diabetics who
    > > have not yet start taking insulin injections?

    >
    > By decreasing levels of inflammatory cytokines which are produced by
    > visceral adipocytes.
    >

    How then there can be a genetic predisposition towards developing
    insulin resistance?

    Whether inflammatory cytokines which are produced by visceral
    adipocytes is only reason to getting IR or all inflammatory responses
    can cause insulin resistance and hyperglycemia(infections are already
    indicated to increse blood glucose levels)?

    As such, can greater adiposity or obesity be treated as inflammatory
    diseases?

    > > > > Will then
    > > > > insulin be normally effective to these new cells?
    > > >
    > > > Not in the setting of metabolic syndrome (MetS).


    Does it indicate that it is due to genetic predisposition?

    ..

    > > > > Can/does insulin polymerize at other comprtments than blood?
    > > >
    > > > Hydrostatic and electrostatic interactions do not involve the formation
    > > > of covalent bonds necessary for polymerization.


    Are there Hydrostatic and electrostatic intermolecular interactions
    between insulin molecules which may keep these molecules
    associated/aggregated enabling these to escape filteration/loss via
    kidneys and stored or act for long time as per need?
    ..
    >
    > The term polymerization, by definition, involves the formation of
    > covalent bonds.


    Yes, thanks.

    > > > > In short does our body has any mechanism by
    > > > > which insulin can be stored and persit for longer time?
    > > >
    > > > No. If it did, insulin would lose its ability to signal.
    > > >

    > > Yes, but on getting diabeteswith IR, it looks alike as insulin is
    > > working lesser.

    >
    > It still works as a signal even if less effectively.


    It works less, whether due to receptor's regulations changes?


    > > > > > > What such more insulin can cause, how it will signal other actions?
    > > > > >
    > > > > > Through its receptors which when activated phosphorylates specific
    > > > > > intracellular proteins involved in increasing glucose uptake and
    > > > > > growth.
    > > > > It looks all actions of insulin is primarily glucose related. Ok?
    > > >
    > > > It also promotes growth.
    > > >

    > > How?

    >
    > Through receptor-mediated post-translational modification (tyrosine
    > phosporylation) of intracellular proteins involved in cellular growth.


    Thanks.
     
  8. Kumar wrote:
    > Andrew B. Chung, MD/PhD wrote:
    > > Kumar wrote:
    > > > Is there any other resistance in transporting injected insulin to
    > > > vascular compartment?

    > >
    > > No.

    >
    > Can insulin molecules in blood or at other compartment be aggregated or
    > associated by intermolecular forces without polymerization?


    Yes.

    > If yes, can
    > this condition exist for long?


    Perhaps if conditions are non-physiological.

    > > > What are these intermolecular interactions?

    > >
    > > Receptor binding.
    > >

    > Good thanks.


    You are welcome :)

    > > > > Actually, there is a genetic predisposition toward developing insulin
    > > > > resistance.
    > > > >
    > > > How then it is reversible by correcting obesity esp.in diabetics who
    > > > have not yet start taking insulin injections?

    > >
    > > By decreasing levels of inflammatory cytokines which are produced by
    > > visceral adipocytes.
    > >

    > How then there can be a genetic predisposition towards developing
    > insulin resistance?


    There are a number of possibilities. One example is that it could
    occur with the genetic predisposition to develop visceral adiposity.

    > Whether inflammatory cytokines which are produced by visceral
    > adipocytes is only reason to getting IR or all inflammatory responses
    > can cause insulin resistance and hyperglycemia(infections are already
    > indicated to increse blood glucose levels)?


    Chronically elevated levels of inflammatory cytokines likely has the
    potential for causing IR regardless of the primary cause.

    > As such, can greater adiposity or obesity be treated as inflammatory
    > diseases?


    Far wiser would be to address the primary reason for the
    adiposity/obesity.

    > > > > > Will then
    > > > > > insulin be normally effective to these new cells?
    > > > >
    > > > > Not in the setting of metabolic syndrome (MetS).

    >
    > Does it indicate that it is due to genetic predisposition?
    >


    There is a genetic predisposition to develop MetS.

    >
    > > > > > Can/does insulin polymerize at other comprtments than blood?
    > > > >
    > > > > Hydrostatic and electrostatic interactions do not involve the formation
    > > > > of covalent bonds necessary for polymerization.

    >
    > Are there Hydrostatic and electrostatic intermolecular interactions
    > between insulin molecules which may keep these molecules
    > associated/aggregated enabling these to escape filteration/loss via
    > kidneys and stored or act for long time as per need?


    Probably not under physiological conditions. Again, insulin is
    catabolized by the kidneys and not excreted.

    > > The term polymerization, by definition, involves the formation of
    > > covalent bonds.

    >
    > Yes, thanks.


    Again, you are welcome.

    > > > > > In short does our body has any mechanism by
    > > > > > which insulin can be stored and persit for longer time?
    > > > >
    > > > > No. If it did, insulin would lose its ability to signal.
    > > > >
    > > > Yes, but on getting diabeteswith IR, it looks alike as insulin is
    > > > working lesser.

    > >
    > > It still works as a signal even if less effectively.

    >
    > It works less, whether due to receptor's regulations changes?


    There is storage of insulin occurring in extracellular compartments.

    > > > > > > > What such more insulin can cause, how it will signal other actions?
    > > > > > >
    > > > > > > Through its receptors which when activated phosphorylates specific
    > > > > > > intracellular proteins involved in increasing glucose uptake and
    > > > > > > growth.
    > > > > > It looks all actions of insulin is primarily glucose related. Ok?
    > > > >
    > > > > It also promotes growth.
    > > > >
    > > > How?

    > >
    > > Through receptor-mediated post-translational modification (tyrosine
    > > phosporylation) of intracellular proteins involved in cellular growth.

    >
    > Thanks.


    You are welcome :)

    All thanks and praises belong to the LORD, Whom I love with all my
    heart, soul, mind, and strength :))

    Will be available to "glow" and chat about this and other things like
    cardiology, diabetes, cooking and nutrition that interest those
    following this thread here during the next on-line chat (02/02/06) from
    6 to 7 pm EST:

    http://tinyurl.com/cpayh

    For those who are put off by the signature, my advance apologies for
    how the LORD has reshaped me:

    http://tinyurl.com/bgfqt

    Prayerfully in Christ's love,

    Andrew
    http://tinyurl.com/8juld
     
  9. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > Andrew B. Chung, MD/PhD wrote:
    > > > Kumar wrote:
    > > > > Is there any other resistance in transporting injected insulin to
    > > > > vascular compartment?
    > > >
    > > > No.

    > >
    > > Can insulin molecules in blood or at other compartment be aggregated or
    > > associated by intermolecular forces without polymerization?

    >
    > Yes.


    Can you tell some more detail about it? What is medical condition named
    for it?

    > > If yes, can
    > > this condition exist for long?

    >
    > Perhaps if conditions are non-physiological.
    >
    > > > > What are these intermolecular interactions?
    > > >
    > > > Receptor binding.
    > > >

    > > Good thanks.

    >
    > You are welcome :)
    >
    > > > > > Actually, there is a genetic predisposition toward developing insulin
    > > > > > resistance.
    > > > > >
    > > > > How then it is reversible by correcting obesity esp.in diabetics who
    > > > > have not yet start taking insulin injections?
    > > >
    > > > By decreasing levels of inflammatory cytokines which are produced by
    > > > visceral adipocytes.
    > > >

    > > How then there can be a genetic predisposition towards developing
    > > insulin resistance?

    >
    > There are a number of possibilities. One example is that it could
    > occur with the genetic predisposition to develop visceral adiposity.


    To get fat depositions or visceral adiposity, whether digestive acidic
    or alkaline secretions and balanced insulin secretions is needed to be
    changed/imbalanced?

    Can low gastric acid, excess bile and low bicarbonate cause excess
    intestinal fats digestion and absorption?
    > > Whether inflammatory cytokines which are produced by visceral
    > > adipocytes is only reason to getting IR or all inflammatory responses
    > > can cause insulin resistance and hyperglycemia(infections are already
    > > indicated to increse blood glucose levels)?

    >
    > Chronically elevated levels of inflammatory cytokines likely has the
    > potential for causing IR regardless of the primary cause.


    Whether Chronically elevated levels of inflammatory cytokines can be
    the only/main cause of getting IR?

    > > As such, can greater adiposity or obesity be treated as inflammatory
    > > diseases?

    >
    > Far wiser would be to address the primary reason for the
    > adiposity/obesity.


    What is that? Is it taking excess glucose/fats?
    > > > > > > Will then
    > > > > > > insulin be normally effective to these new cells?
    > > > > >
    > > > > > Not in the setting of metabolic syndrome (MetS).

    > >
    > > Does it indicate that it is due to genetic predisposition?
    > >

    >
    > There is a genetic predisposition to develop MetS.


    Can genetic predisostions in diabetes2 basically cause excess cravings
    to foods resulting into more food intake>>more glucose>>more
    insulin>>IR>>hyperglycemia....?

    If yes, how this excess craving is oriented? Is it by genetic
    predisposition to get excess gastric acid and insulin secretion?
    > >
    > > > > > > Can/does insulin polymerize at other comprtments than blood?
    > > > > >
    > > > > > Hydrostatic and electrostatic interactions do not involve the formation
    > > > > > of covalent bonds necessary for polymerization.

    > >
    > > Are there Hydrostatic and electrostatic intermolecular interactions
    > > between insulin molecules which may keep these molecules
    > > associated/aggregated enabling these to escape filteration/loss via
    > > kidneys and stored or act for long time as per need?

    >
    > Probably not under physiological conditions.


    Whether diabetes or persisting hyperglycemia is a physiological
    conditions?

    Can't aggregation/assotiation or concentration of insulin molecules by
    Hydrostatic and electrostatic intermolecular interactions AND by its
    oligomerization be a natural body mechanism to control/balance/maintain
    and store(either of these) insulin levels in blood--aggregation
    somewhat medium acting and oligomerization somewhat long acting?

    >Again, insulin is
    > catabolized by the kidneys and not excreted.


    Does it mean that it is filtered and lost its origional form as
    degraded/denatured in kidneys(in loosing i am not counting reabsorption
    of degraded/denatured form)? Or, it is degraded/denatured at other
    parts(say liver) and filtered and lost in its degraded/denatured form?

    > > > The term polymerization, by definition, involves the formation of
    > > > covalent bonds.

    > >
    > > Yes, thanks.

    >
    > Again, you are welcome.
    >
    > > > > > > In short does our body has any mechanism by
    > > > > > > which insulin can be stored and persit for longer time?
    > > > > >
    > > > > > No. If it did, insulin would lose its ability to signal.
    > > > > >
    > > > > Yes, but on getting diabeteswith IR, it looks alike as insulin is
    > > > > working lesser.
    > > >
    > > > It still works as a signal even if less effectively.

    > >


    Whether insulin loosing its ability to signal is due to aggregation of
    its molecules?

    > > It works less, whether due to receptor's regulations changes?

    >
    > There is storage of insulin occurring in extracellular compartments.


    How and in what form of insulin?

    > > > > > > > > What such more insulin can cause, how it will signal other actions?
    > > > > > > >
    > > > > > > > Through its receptors which when activated phosphorylates specific
    > > > > > > > intracellular proteins involved in increasing glucose uptake and
    > > > > > > > growth.
    > > > > > > It looks all actions of insulin is primarily glucose related. Ok?
    > > > > >
    > > > > > It also promotes growth.
    > > > > >
    > > > > How?
    > > >
    > > > Through receptor-mediated post-translational modification (tyrosine
    > > > phosporylation) of intracellular proteins involved in cellular growth.

    > >
    > > Thanks.

    >
    > You are welcome :)
    >

    You deserve. All people esp. those who accept sprituals+science belong
    to LORD. We know we have spritual+scientific OR
    sensations/psychlogical+ingestion/chemical/physiological effects OR
    (cephalic+ingestion..pre-stomach+in stomach andpost-stomach) effects
    but still we think less of sprituals.
    > All thanks and praises belong to the LORD, Whom I love with all my
    > heart, soul, mind, and strength :))
    >
    > Will be available to "glow" and chat about this and other things like
    > cardiology, diabetes, cooking and nutrition that interest those
    > following this thread here during the next on-line chat (02/02/06) from
    > 6 to 7 pm EST:
    >
    > http://tinyurl.com/cpayh
    >
    > For those who are put off by the signature, my advance apologies for
    > how the LORD has reshaped me:
    >
    > http://tinyurl.com/bgfqt
    >
    > Prayerfully in Christ's love,
    >
    > Andrew
    > http://tinyurl.com/8juld
     
  10. Kumar wrote:
    > Andrew B. Chung, MD/PhD wrote:
    > > Kumar wrote:
    > > > Andrew B. Chung, MD/PhD wrote:
    > > > > Kumar wrote:
    > > > > > Is there any other resistance in transporting injected insulin to
    > > > > > vascular compartment?
    > > > >
    > > > > No.
    > > >
    > > > Can insulin molecules in blood or at other compartment be aggregated or
    > > > associated by intermolecular forces without polymerization?

    > >
    > > Yes.

    >
    > Can you tell some more detail about it? What is medical condition named
    > for it?


    Death (ie non-physiological)

    > > > If yes, can
    > > > this condition exist for long?

    > >
    > > Perhaps if conditions are non-physiological.
    > >
    > > > > > What are these intermolecular interactions?
    > > > >
    > > > > Receptor binding.
    > > > >
    > > > Good thanks.

    > >
    > > You are welcome :)
    > >
    > > > > > > Actually, there is a genetic predisposition toward developing insulin
    > > > > > > resistance.
    > > > > > >
    > > > > > How then it is reversible by correcting obesity esp.in diabetics who
    > > > > > have not yet start taking insulin injections?
    > > > >
    > > > > By decreasing levels of inflammatory cytokines which are produced by
    > > > > visceral adipocytes.
    > > > >
    > > > How then there can be a genetic predisposition towards developing
    > > > insulin resistance?

    > >
    > > There are a number of possibilities. One example is that it could
    > > occur with the genetic predisposition to develop visceral adiposity.

    >
    > To get fat depositions or visceral adiposity, whether digestive acidic
    > or alkaline secretions and balanced insulin secretions is needed to be
    > changed/imbalanced?


    Overeating is necessary and sufficient for developing visceral
    adiposity.

    > Can low gastric acid, excess bile and low bicarbonate cause excess
    > intestinal fats digestion and absorption?


    Not when there has been no excess ingested.

    > > > Whether inflammatory cytokines which are produced by visceral
    > > > adipocytes is only reason to getting IR or all inflammatory responses
    > > > can cause insulin resistance and hyperglycemia(infections are already
    > > > indicated to increse blood glucose levels)?

    > >
    > > Chronically elevated levels of inflammatory cytokines likely has the
    > > potential for causing IR regardless of the primary cause.

    >
    > Whether Chronically elevated levels of inflammatory cytokines can be
    > the only/main cause of getting IR?


    It is the only cause we know of at the moment.

    > > > As such, can greater adiposity or obesity be treated as inflammatory
    > > > diseases?

    > >
    > > Far wiser would be to address the primary reason for the
    > > adiposity/obesity.

    >
    > What is that? Is it taking excess glucose/fats?


    Overeating.

    > > > > > > > Will then
    > > > > > > > insulin be normally effective to these new cells?
    > > > > > >
    > > > > > > Not in the setting of metabolic syndrome (MetS).
    > > >
    > > > Does it indicate that it is due to genetic predisposition?
    > > >

    > >
    > > There is a genetic predisposition to develop MetS.

    >
    > Can genetic predisostions in diabetes2 basically cause excess cravings
    > to foods resulting into more food intake>>more glucose>>more
    > insulin>>IR>>hyperglycemia....?


    No. It lowers the threshold of amount of visceral adiposity before IR
    occurs.

    > If yes, how this excess craving is oriented? Is it by genetic
    > predisposition to get excess gastric acid and insulin secretion?


    No.

    > > > > > > > Can/does insulin polymerize at other comprtments than blood?
    > > > > > >
    > > > > > > Hydrostatic and electrostatic interactions do not involve the formation
    > > > > > > of covalent bonds necessary for polymerization.
    > > >
    > > > Are there Hydrostatic and electrostatic intermolecular interactions
    > > > between insulin molecules which may keep these molecules
    > > > associated/aggregated enabling these to escape filteration/loss via
    > > > kidneys and stored or act for long time as per need?

    > >
    > > Probably not under physiological conditions.

    >
    > Whether diabetes or persisting hyperglycemia is a physiological
    > conditions?


    In the absence of DKA, the conditions should remain physiological
    through mechanisms that maintain homeostasis.

    > Can't aggregation/assotiation or concentration of insulin molecules by
    > Hydrostatic and electrostatic intermolecular interactions AND by its
    > oligomerization be a natural body mechanism to control/balance/maintain
    > and store(either of these) insulin levels in blood--aggregation
    > somewhat medium acting and oligomerization somewhat long acting?


    No. Again, storage of insulin would disrupt its signalling function.

    > >Again, insulin is
    > > catabolized by the kidneys and not excreted.

    >
    > Does it mean that it is filtered and lost its origional form as
    > degraded/denatured in kidneys(in loosing i am not counting reabsorption
    > of degraded/denatured form)? Or, it is degraded/denatured at other
    > parts(say liver) and filtered and lost in its degraded/denatured form?


    It simply is not excreted but catabolized.

    > > > > The term polymerization, by definition, involves the formation of
    > > > > covalent bonds.
    > > >
    > > > Yes, thanks.

    > >
    > > Again, you are welcome.
    > >
    > > > > > > > In short does our body has any mechanism by
    > > > > > > > which insulin can be stored and persit for longer time?
    > > > > > >
    > > > > > > No. If it did, insulin would lose its ability to signal.
    > > > > > >
    > > > > > Yes, but on getting diabeteswith IR, it looks alike as insulin is
    > > > > > working lesser.
    > > > >
    > > > > It still works as a signal even if less effectively.
    > > >

    >
    > Whether insulin loosing its ability to signal is due to aggregation of
    > its molecules?


    No. It occurs by a downregulation of its receptor number because of
    the action of inflammatory cytokines.

    > > > It works less, whether due to receptor's regulations changes?

    > >
    > > There is storage of insulin occurring in extracellular compartments.

    >
    > How and in what form of insulin?


    Sorry. That should have been that there is **no** storage of insulin
    in extracellular compartments. There is storage of pro-insulin in
    intracellular compartments.

    > > > > > > > > > What such more insulin can cause, how it will signal other actions?
    > > > > > > > >
    > > > > > > > > Through its receptors which when activated phosphorylates specific
    > > > > > > > > intracellular proteins involved in increasing glucose uptake and
    > > > > > > > > growth.
    > > > > > > > It looks all actions of insulin is primarily glucose related. Ok?
    > > > > > >
    > > > > > > It also promotes growth.
    > > > > > >
    > > > > > How?
    > > > >
    > > > > Through receptor-mediated post-translational modification (tyrosine
    > > > > phosporylation) of intracellular proteins involved in cellular growth.
    > > >
    > > > Thanks.

    > >
    > > You are welcome :)
    > >

    > You deserve.


    I deserve nothing but have been blessed with much through the LORD's
    infinite mercy and grace.

    However, thank you for the kind thoughts.

    May the LORD bless you and yours today and everyday, in Jesus' most
    precious and holy name :)

    Will be available to "glow" and chat about this and other things like
    cardiology, diabetes, cooking and nutrition that interest those
    following this thread here during the next on-line chat (02/02/06) from
    6 to 7 pm EST:

    http://tinyurl.com/cpayh

    For those who are put off by the signature, my advance apologies for
    how the LORD has reshaped me:

    http://tinyurl.com/bgfqt

    Prayerfully in Christ's love,

    Andrew
    http://tinyurl.com/8juld
     
  11. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > Andrew B. Chung, MD/PhD wrote:
    > > > Kumar wrote:
    > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > Kumar wrote:
    > > > > > > Is there any other resistance in transporting injected insulin to
    > > > > > > vascular compartment?
    > > > > >
    > > > > > No.
    > > > >
    > > > > Can insulin molecules in blood or at other compartment be aggregated or
    > > > > associated by intermolecular forces without polymerization?
    > > >
    > > > Yes.

    > >
    > > Can you tell some more detail about it? What is medical condition named
    > > for it?

    >
    > Death (ie non-physiological)
    >


    What about in physiological imbalances? Can't something be other than
    physiological and non-physiological? I consider it as physiological
    imbalances as in diabetes, IR etc.
    > > > > If yes, can
    > > > > this condition exist for long?
    > > >
    > > > Perhaps if conditions are non-physiological.
    > > >
    > > > > > > What are these intermolecular interactions?
    > > > > >
    > > > > > Receptor binding.
    > > > > >
    > > > > Good thanks.
    > > >
    > > > You are welcome :)
    > > >
    > > > > > > > Actually, there is a genetic predisposition toward developing insulin
    > > > > > > > resistance.
    > > > > > > >
    > > > > > > How then it is reversible by correcting obesity esp.in diabetics who
    > > > > > > have not yet start taking insulin injections?
    > > > > >
    > > > > > By decreasing levels of inflammatory cytokines which are produced by
    > > > > > visceral adipocytes.
    > > > > >
    > > > > How then there can be a genetic predisposition towards developing
    > > > > insulin resistance?
    > > >
    > > > There are a number of possibilities. One example is that it could
    > > > occur with the genetic predisposition to develop visceral adiposity.

    > >
    > > To get fat depositions or visceral adiposity, whether digestive acidic
    > > or alkaline secretions and balanced insulin secretions is needed to be
    > > changed/imbalanced?

    >
    > Overeating is necessary and sufficient for developing visceral
    > adiposity.


    Yes, but on overeating, can't imbalances in gastric acid, bile or
    bicarbonate cause more or less digestions resulting into more or less
    absoptions of fats?
    >
    > > Can low gastric acid, excess bile and low bicarbonate cause excess
    > > intestinal fats digestion and absorption?

    >
    > Not when there has been no excess ingested.


    Oh you awnsered. It can be more or less due to digestive secretions?
    >
    > > > > Whether inflammatory cytokines which are produced by visceral
    > > > > adipocytes is only reason to getting IR or all inflammatory responses
    > > > > can cause insulin resistance and hyperglycemia(infections are already
    > > > > indicated to increse blood glucose levels)?
    > > >
    > > > Chronically elevated levels of inflammatory cytokines likely has the
    > > > potential for causing IR regardless of the primary cause.

    > >
    > > Whether Chronically elevated levels of inflammatory cytokines can be
    > > the only/main cause of getting IR?

    >
    > It is the only cause we know of at the moment.


    Thanks. Iron imbalances and relaxed conditions of blood
    vessels(dilation) (may be swelling,acidosis,pain) look to be related to
    inflammatory diseases. How these conditions can be related to adiposity
    and getting inflammatory cytolines?
    >
    > > > > As such, can greater adiposity or obesity be treated as inflammatory
    > > > > diseases?
    > > >
    > > > Far wiser would be to address the primary reason for the
    > > > adiposity/obesity.

    > >
    > > What is that? Is it taking excess glucose/fats?

    >
    > Overeating.
    >

    Can exposure of various foods, easy cooking, easy availabilty of foods,
    stress i.e. modern lifestyle in big cities and pollution can cause
    excess cravings and overeating? If yes, will these cause excess gastric
    acid and insulin secretions by somewhat "cephalic phase type effects?
    Probably alike use of double bads may trigger readymade and excessive
    urge to sit and sleep.

    Accordingly are we either genetically predisposed to make such modern
    lifestyle etc. imbalances or genetic predispositions in body's cells
    towords getting the diseases? (just a thought).
    > > > > > > > > Will then
    > > > > > > > > insulin be normally effective to these new cells?
    > > > > > > >
    > > > > > > > Not in the setting of metabolic syndrome (MetS).
    > > > >
    > > > > Does it indicate that it is due to genetic predisposition?
    > > > >
    > > >
    > > > There is a genetic predisposition to develop MetS.

    > >
    > > Can genetic predisostions in diabetes2 basically cause excess cravings
    > > to foods resulting into more food intake>>more glucose>>more
    > > insulin>>IR>>hyperglycemia....?

    >
    > No. It lowers the threshold of amount of visceral adiposity before IR
    > occurs.
    >

    Yes but how? Whether visceral adiposity is a natural body response to
    protect organs in inflammatory conditions?

    > > If yes, how this excess craving is oriented? Is it by genetic
    > > predisposition to get excess gastric acid and insulin secretion?

    >
    > No.
    >


    Or as above which I mentioned..modern lifestyle and atmosphere?

    Btw, how getting diabetes2, IR and hypertentions are different in big
    polluted and crowded cities and in clean environment remote and natural
    areas of small villages or in jungles?
    > > > > > > > > Can/does insulin polymerize at other comprtments than blood?
    > > > > > > >
    > > > > > > > Hydrostatic and electrostatic interactions do not involve the formation
    > > > > > > > of covalent bonds necessary for polymerization.
    > > > >
    > > > > Are there Hydrostatic and electrostatic intermolecular interactions
    > > > > between insulin molecules which may keep these molecules
    > > > > associated/aggregated enabling these to escape filteration/loss via
    > > > > kidneys and stored or act for long time as per need?
    > > >
    > > > Probably not under physiological conditions.

    > >
    > > Whether diabetes or persisting hyperglycemia is a physiological
    > > conditions?

    >
    > In the absence of DKA, the conditions should remain physiological
    > through mechanisms that maintain homeostasis.
    >

    Yes but what about maintainable imbalances or in "not yet fatal"
    conditions? We can have persistent hyperglycemia, fats depositions etc.
    for many years still may not be "immediate fatal". I think these can be
    catagerized as "physiological imbalances" instead of physiological or
    non-physiological. ??
    > > Can't aggregation/assotiation or concentration of insulin molecules by
    > > Hydrostatic and electrostatic intermolecular interactions AND by its
    > > oligomerization be a natural body mechanism to control/balance/maintain
    > > and store(either of these) insulin levels in blood--aggregation
    > > somewhat medium acting and oligomerization somewhat long acting?

    >
    > No. Again, storage of insulin would disrupt its signalling function.
    >


    Yes, but some insulin can be stored for prolonged requirements due to
    persitent hyperglycemia. This looks alike IR.

    Btw, whether pacreas can continuously secrete insulin or need some time
    to refill--in normal health and in diabetes2?


    > > >Again, insulin is
    > > > catabolized by the kidneys and not excreted.

    > >
    > > Does it mean that it is filtered and lost its origional form as
    > > degraded/denatured in kidneys(in loosing i am not counting reabsorption
    > > of degraded/denatured form)? Or, it is degraded/denatured at other
    > > parts(say liver) and filtered and lost in its degraded/denatured form?

    >
    > It simply is not excreted but catabolized.
    >

    Ok, it looks like suspense. Cells uses insulin in kidney's area is a
    different aspect but whether some insulin in reasonable quantity
    effecting glucose levels in blood is lost via kidneys or not in normal
    health or in some disease?

    > > > > > The term polymerization, by definition, involves the formation of
    > > > > > covalent bonds.
    > > > >
    > > > > Yes, thanks.
    > > >
    > > > Again, you are welcome.
    > > >
    > > > > > > > > In short does our body has any mechanism by
    > > > > > > > > which insulin can be stored and persit for longer time?
    > > > > > > >
    > > > > > > > No. If it did, insulin would lose its ability to signal.
    > > > > > > >
    > > > > > > Yes, but on getting diabeteswith IR, it looks alike as insulin is
    > > > > > > working lesser.
    > > > > >
    > > > > > It still works as a signal even if less effectively.
    > > > >

    > >
    > > Whether insulin loosing its ability to signal is due to aggregation of
    > > its molecules?

    >
    > No. It occurs by a downregulation of its receptor number because of
    > the action of inflammatory cytokines.
    >

    Yes, thanks. Is there any medicine which can directly control these
    inflammatory cytokines without controlling adiposity? NSAIDs??
    > > > > It works less, whether due to receptor's regulations changes?
    > > >
    > > > There is storage of insulin occurring in extracellular compartments.

    > >
    > > How and in what form of insulin?

    >
    > Sorry. That should have been that there is **no** storage of insulin
    > in extracellular compartments. There is storage of pro-insulin in
    > intracellular compartments.
    >

    Ok, it shoked me at that time. Storage of pro-insulin in Intracellular
    compartments--you mean only in pancreas?
    >
    > > > > > > > > > What such more insulin can cause, how it will signal

    other actions?
    > > > > > > > > >
    > > > > > > > > > Through its receptors which when activated phosphorylates specific
    > > > > > > > > > intracellular proteins involved in increasing glucose uptake and
    > > > > > > > > > growth.
    > > > > > > > > It looks all actions of insulin is primarily glucose related. Ok?
    > > > > > > >
    > > > > > > > It also promotes growth.
    > > > > > > >
    > > > > > > How?
    > > > > >
    > > > > > Through receptor-mediated post-translational modification (tyrosine
    > > > > > phosporylation) of intracellular proteins involved in cellular growth.
    > > > >
    > > > > Thanks.
    > > >
    > > > You are welcome :)
    > > >

    > > You deserve.

    >
    > I deserve nothing but have been blessed with much through the LORD's
    > infinite mercy and grace.
    >
    > However, thank you for the kind thoughts.
    >
    > May the LORD bless you and yours today and everyday, in Jesus' most
    > precious and holy name :)
    >

    Thanks for your kind blessings.

    > Will be available to "glow" and chat about this and other things like
    > cardiology, diabetes, cooking and nutrition that interest those
    > following this thread here during the next on-line chat (02/02/06) from
    > 6 to 7 pm EST:
    >
    > http://tinyurl.com/cpayh
    >
    > For those who are put off by the signature, my advance apologies for
    > how the LORD has reshaped me:
    >
    > http://tinyurl.com/bgfqt
    >
    > Prayerfully in Christ's love,
    >
    > Andrew
    > http://tinyurl.com/8juld
     
  12. John

    John Guest

    On Sat, 28 Jan 2006 08:29:33 -0600, "Ken Kubos" <[email protected]>
    wrote:

    >Aaaaah the lord made an obsessive-compulsive (http://www.ocfoundation.org/)
    >little man!
    >Ken
    >
    >"Buddhism elucidates why we are sentient."
    >"Karma means that you don't get away with anything."


    Being made in God's image explains our sentience.

    God's Grace means that we can "get away with" everything, provided
    that we accept that Grace through Jesus Christ and are truly
    repentant.

    John
     
  13. John wrote:
    > On Sat, 28 Jan 2006 08:29:33 -0600, "Ken Kubos" <[email protected]>
    > wrote:
    >
    > >Aaaaah the lord made an obsessive-compulsive (http://www.ocfoundation.org/)
    > >little man!
    > >Ken
    > >
    > >"Buddhism elucidates why we are sentient."
    > >"Karma means that you don't get away with anything."

    >
    > Being made in God's image explains our sentience.
    >
    > God's Grace means that we can "get away with" everything, provided
    > that we accept that Grace through Jesus Christ and are truly
    > repentant.
    >
    > John


    Amen and amen :)

    May the LORD continue to bless you and yours today and everyday, in
    Jesus' most precious and holy name :))

    Will be available to "glow" and chat about this and other things like
    cardiology, diabetes, cooking and nutrition that interest those
    following this thread here during the next on-line chat (02/02/06) from
    6 to 7 pm EST:

    http://tinyurl.com/cpayh

    For those who are put off by the signature, my advance apologies for
    how the LORD has reshaped me:

    http://tinyurl.com/bgfqt

    Prayerfully in Christ's love,

    Andrew
    http://tinyurl.com/8juld
     
  14. Kumar

    Kumar Guest

    "Fat-Immune System-Inflammation Link
    Your fat cells increase inflammation in another way, by attracting a
    type of white blood cell known as a macrophage, which produces
    inflammatory cytokines.(9) Macrophages are scavenger cells. Their job
    is literally to gobble up foreign organisms and cellular debris.

    Macrophages seem to be drawn to body fat because fat cells tend to leak
    and break open, especially in people with abdominal obesity.
    Macrophages move into the leaky fat tissue in order to clean up debris
    and then they themselves begin to release inflammatory factors.
    Macrophages appear to be a major contributor to inflammation.(
    the relationship of diet, inflammation and weight is summarized here:

    A diet high in refined carbohydrates and other "fabricated" foods leads
    to both increased weight and increased inflammation.

    Excess weight itself causes chronic inflammation.

    Chronic inflammation contributes to more insulin resistance, leptin
    resistance, and other metabolic disorders. It also decreases favorable
    adiponectin and increases unfavorable resistin.

    Insulin resistance and leptin resistance stimulate accumulation of more
    weight, make weight loss more difficult, and induce hyperandrogenism
    (excessive levels of male hormones) and other symptoms of PCOS.

    The added weight induces more inflammation and thus more insulin and
    leptin resistance, which in turn prevents you from burning off fat
    stores, and causes you to store even more fat.
    Here is the vicious cycle of obesity and leptin resistance: Extra fat
    produces chronic, low-grade inflammation. The chronic inflammation
    produces a chronic anti-inflammatory response, led by SOCS molecules.
    The SOCS response stops leptin from reducing obesity. So weight goes
    up, which causes more inflammation. And the cycle starts all over
    again.
    http://www.ovarian-cysts-pcos.com/inflammation.html#sec2 "

    Whether IR happens in the way as mentioned on above link?
     
  15. Kumar

    Kumar Guest

    "In a normal person, a small amount of insulin is produced after eating
    ("postprandial"), and it signals the body to absorb the sugars from the
    food at a steady rate. In an "insulin resistant" person the message
    does not get to the cells so the sugar remains in the blood for long
    periods of time while ever more insulin is released in an attempt to
    trigger the sugar-uptake. The sugar circulates in the blood for several
    hours and then is taken into the cells very rapidly, leading to a steep
    drop in blood sugar and a hypoglycaemic reaction several hours after
    the meal.

    At a later stage, frank hyperglycemia develops as pancreatic ß-cells
    are unable to produce adequate insulin to maintain normal blood sugar
    levels ("euglycemia").


    Various disease states make the body tissues more resistant to the
    actions of insulin. Example include infection (TNFa) and acidosis.
    Recent research involves the relative roles of adipokines (the
    cytokines produced by adipose tissue) in modifying insulin resistance
    http://en.wikipedia.org/wiki/Insulin_resistance "

    Glucose requirements may be more in case of getting infections and
    inflammations. Infections and greater adiposity trigger inflammatory
    responses so more need of energy/glucose. So these inflammatory
    responses are meant to remove the cause of inflammations--adiposity anf
    infections.

    Can't such inflammatory responses treat greater adiposity, infections
    etc. naturally? In view of this, How far it is correct to lower such
    hyperglycemia by medications instead of correcting greater adiposity,
    infections or inflammatory responses? Can't such interferances by
    medications will not interfere in the natural treatment of these
    inflammatory responses? What can be the results of such interferances
    by medications?
     
  16. Kumar wrote:
    > Andrew B. Chung, MD/PhD wrote:
    > > Kumar wrote:
    > > > Andrew B. Chung, MD/PhD wrote:
    > > > > Kumar wrote:
    > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > Kumar wrote:
    > > > > > > > Is there any other resistance in transporting injected insulin to
    > > > > > > > vascular compartment?
    > > > > > >
    > > > > > > No.
    > > > > >
    > > > > > Can insulin molecules in blood or at other compartment be aggregated or
    > > > > > associated by intermolecular forces without polymerization?
    > > > >
    > > > > Yes.
    > > >
    > > > Can you tell some more detail about it? What is medical condition named
    > > > for it?

    > >
    > > Death (ie non-physiological)
    > >

    >
    > What about in physiological imbalances? Can't something be other than
    > physiological and non-physiological?


    Yes... unstable.

    > I consider it as physiological
    > imbalances as in diabetes, IR etc.


    Chronic conditions still result in a steady-state (homeostasis) which
    will be physiological.

    > > > > > If yes, can
    > > > > > this condition exist for long?
    > > > >
    > > > > Perhaps if conditions are non-physiological.
    > > > >
    > > > > > > > What are these intermolecular interactions?
    > > > > > >
    > > > > > > Receptor binding.
    > > > > > >
    > > > > > Good thanks.
    > > > >
    > > > > You are welcome :)
    > > > >
    > > > > > > > > Actually, there is a genetic predisposition toward developing insulin
    > > > > > > > > resistance.
    > > > > > > > >
    > > > > > > > How then it is reversible by correcting obesity esp.in diabetics who
    > > > > > > > have not yet start taking insulin injections?
    > > > > > >
    > > > > > > By decreasing levels of inflammatory cytokines which are produced by
    > > > > > > visceral adipocytes.
    > > > > > >
    > > > > > How then there can be a genetic predisposition towards developing
    > > > > > insulin resistance?
    > > > >
    > > > > There are a number of possibilities. One example is that it could
    > > > > occur with the genetic predisposition to develop visceral adiposity.
    > > >
    > > > To get fat depositions or visceral adiposity, whether digestive acidic
    > > > or alkaline secretions and balanced insulin secretions is needed to be
    > > > changed/imbalanced?

    > >
    > > Overeating is necessary and sufficient for developing visceral
    > > adiposity.

    >
    > Yes, but on overeating, can't imbalances in gastric acid, bile or
    > bicarbonate cause more or less digestions resulting into more or less
    > absoptions of fats?


    In practice, no.

    > > > Can low gastric acid, excess bile and low bicarbonate cause excess
    > > > intestinal fats digestion and absorption?

    > >
    > > Not when there has been no excess ingested.

    >
    > Oh you awnsered. It can be more or less due to digestive secretions?


    In practice, no.

    > > > > > Whether inflammatory cytokines which are produced by visceral
    > > > > > adipocytes is only reason to getting IR or all inflammatory responses
    > > > > > can cause insulin resistance and hyperglycemia(infections are already
    > > > > > indicated to increse blood glucose levels)?
    > > > >
    > > > > Chronically elevated levels of inflammatory cytokines likely has the
    > > > > potential for causing IR regardless of the primary cause.
    > > >
    > > > Whether Chronically elevated levels of inflammatory cytokines can be
    > > > the only/main cause of getting IR?

    > >
    > > It is the only cause we know of at the moment.

    >
    > Thanks. Iron imbalances and relaxed conditions of blood
    > vessels(dilation) (may be swelling,acidosis,pain) look to be related to
    > inflammatory diseases. How these conditions can be related to adiposity
    > and getting inflammatory cytolines?


    You are mixing up acute with chronic conditions.

    > > > > > As such, can greater adiposity or obesity be treated as inflammatory
    > > > > > diseases?
    > > > >
    > > > > Far wiser would be to address the primary reason for the
    > > > > adiposity/obesity.
    > > >
    > > > What is that? Is it taking excess glucose/fats?

    > >
    > > Overeating.
    > >

    > Can exposure of various foods, easy cooking, easy availabilty of foods,
    > stress i.e. modern lifestyle in big cities and pollution can cause
    > excess cravings and overeating?


    Healthy people have healthy appetites (hunger and cravings).

    Those who are afraid of hunger tend to overeat.

    Those who are not afraid of hunger are able to avoid overeating.

    The latter state of befriending hunger is an enlightened choice.

    > If yes, will these cause excess gastric
    > acid and insulin secretions by somewhat "cephalic phase type effects?
    > Probably alike use of double bads may trigger readymade and excessive
    > urge to sit and sleep.
    >
    > Accordingly are we either genetically predisposed to make such modern
    > lifestyle etc. imbalances or genetic predispositions in body's cells
    > towords getting the diseases? (just a thought).


    Overeating is a choice made out of fear of hunger.

    > > > > > > > > > Will then
    > > > > > > > > > insulin be normally effective to these new cells?
    > > > > > > > >
    > > > > > > > > Not in the setting of metabolic syndrome (MetS).
    > > > > >
    > > > > > Does it indicate that it is due to genetic predisposition?
    > > > > >
    > > > >
    > > > > There is a genetic predisposition to develop MetS.
    > > >
    > > > Can genetic predisostions in diabetes2 basically cause excess cravings
    > > > to foods resulting into more food intake>>more glucose>>more
    > > > insulin>>IR>>hyperglycemia....?

    > >
    > > No. It lowers the threshold of amount of visceral adiposity before IR
    > > occurs.
    > >

    > Yes but how?


    Through insulin receptor number, insulin binding affinity, baseline
    levels of inflammatory cytokines, second messenger signalling pathways,
    gene regulatory promoter elements, etc.

    > Whether visceral adiposity is a natural body response to
    > protect organs in inflammatory conditions?


    No. Visceral adiposity is an unnatural condition arising from
    overeating.

    > > > If yes, how this excess craving is oriented? Is it by genetic
    > > > predisposition to get excess gastric acid and insulin secretion?

    > >
    > > No.
    > >

    >
    > Or as above which I mentioned..modern lifestyle and atmosphere?


    No. Hunger is a healthy state.

    > Btw, how getting diabetes2, IR and hypertentions are different in big
    > polluted and crowded cities and in clean environment remote and natural
    > areas of small villages or in jungles?


    No difference.

    > > > > > > > > > Can/does insulin polymerize at other comprtments than blood?
    > > > > > > > >
    > > > > > > > > Hydrostatic and electrostatic interactions do not involve the formation
    > > > > > > > > of covalent bonds necessary for polymerization.
    > > > > >
    > > > > > Are there Hydrostatic and electrostatic intermolecular interactions
    > > > > > between insulin molecules which may keep these molecules
    > > > > > associated/aggregated enabling these to escape filteration/loss via
    > > > > > kidneys and stored or act for long time as per need?
    > > > >
    > > > > Probably not under physiological conditions.
    > > >
    > > > Whether diabetes or persisting hyperglycemia is a physiological
    > > > conditions?

    > >
    > > In the absence of DKA, the conditions should remain physiological
    > > through mechanisms that maintain homeostasis.
    > >

    > Yes but what about maintainable imbalances or in "not yet fatal"
    > conditions?


    Imbalances are not sustainable.

    > We can have persistent hyperglycemia, fats depositions etc.
    > for many years still may not be "immediate fatal". I think these can be
    > catagerized as "physiological imbalances" instead of physiological or
    > non-physiological. ??


    No.

    > > > Can't aggregation/assotiation or concentration of insulin molecules by
    > > > Hydrostatic and electrostatic intermolecular interactions AND by its
    > > > oligomerization be a natural body mechanism to control/balance/maintain
    > > > and store(either of these) insulin levels in blood--aggregation
    > > > somewhat medium acting and oligomerization somewhat long acting?

    > >
    > > No. Again, storage of insulin would disrupt its signalling function.
    > >

    >
    > Yes, but some insulin can be stored for prolonged requirements due to
    > persitent hyperglycemia. This looks alike IR.


    No.

    > Btw, whether pacreas can continuously secrete insulin or need some time
    > to refill--in normal health and in diabetes2?


    The former.

    >
    > > > >Again, insulin is
    > > > > catabolized by the kidneys and not excreted.
    > > >
    > > > Does it mean that it is filtered and lost its origional form as
    > > > degraded/denatured in kidneys(in loosing i am not counting reabsorption
    > > > of degraded/denatured form)? Or, it is degraded/denatured at other
    > > > parts(say liver) and filtered and lost in its degraded/denatured form?

    > >
    > > It simply is not excreted but catabolized.
    > >

    > Ok, it looks like suspense. Cells uses insulin in kidney's area is a
    > different aspect but whether some insulin in reasonable quantity
    > effecting glucose levels in blood is lost via kidneys or not in normal
    > health or in some disease?


    There is no excretion of insulin by the kidneys. Intact insulin
    polypeptide molecules are not present in the urine in significant
    amounts in normal people.

    > > > > > > The term polymerization, by definition, involves the formation of
    > > > > > > covalent bonds.
    > > > > >
    > > > > > Yes, thanks.
    > > > >
    > > > > Again, you are welcome.
    > > > >
    > > > > > > > > > In short does our body has any mechanism by
    > > > > > > > > > which insulin can be stored and persit for longer time?
    > > > > > > > >
    > > > > > > > > No. If it did, insulin would lose its ability to signal.
    > > > > > > > >
    > > > > > > > Yes, but on getting diabeteswith IR, it looks alike as insulin is
    > > > > > > > working lesser.
    > > > > > >
    > > > > > > It still works as a signal even if less effectively.
    > > > > >
    > > >
    > > > Whether insulin loosing its ability to signal is due to aggregation of
    > > > its molecules?

    > >
    > > No. It occurs by a downregulation of its receptor number because of
    > > the action of inflammatory cytokines.
    > >

    > Yes, thanks. Is there any medicine which can directly control these
    > inflammatory cytokines without controlling adiposity?


    No.

    > NSAIDs??


    No.

    Why look for medicine when permanent weight loss cures this?

    http://www.HeartMDPhD.com/wtloss.asp

    > > > > > It works less, whether due to receptor's regulations changes?
    > > > >
    > > > > There is storage of insulin occurring in extracellular compartments.
    > > >
    > > > How and in what form of insulin?

    > >
    > > Sorry. That should have been that there is **no** storage of insulin
    > > in extracellular compartments. There is storage of pro-insulin in
    > > intracellular compartments.
    > >

    > Ok, it shoked me at that time. Storage of pro-insulin in Intracellular
    > compartments--you mean only in pancreas?


    Specifically, only in the beta islet cells of the pancreas.

    > > > > > > > > > > What such more insulin can cause, how it will signal

    > other actions?
    > > > > > > > > > >
    > > > > > > > > > > Through its receptors which when activated phosphorylates specific
    > > > > > > > > > > intracellular proteins involved in increasing glucose uptake and
    > > > > > > > > > > growth.
    > > > > > > > > > It looks all actions of insulin is primarily glucose related. Ok?
    > > > > > > > >
    > > > > > > > > It also promotes growth.
    > > > > > > > >
    > > > > > > > How?
    > > > > > >
    > > > > > > Through receptor-mediated post-translational modification (tyrosine
    > > > > > > phosporylation) of intracellular proteins involved in cellular growth.
    > > > > >
    > > > > > Thanks.
    > > > >
    > > > > You are welcome :)
    > > > >
    > > > You deserve.

    > >
    > > I deserve nothing but have been blessed with much through the LORD's
    > > infinite mercy and grace.
    > >
    > > However, thank you for the kind thoughts.
    > >
    > > May the LORD bless you and yours today and everyday, in Jesus' most
    > > precious and holy name :)
    > >

    > Thanks for your kind blessings.


    The blessings are HIS.

    All thanks and praises belong to the LORD, Whom I love with all my
    heart, soul, mind, and strength :))

    Will be available to "glow" and chat about this and other things like
    cardiology, diabetes, cooking and nutrition that interest those
    following this thread here during the next on-line chat (02/02/06) from
    6 to 7 pm EST:

    http://tinyurl.com/cpayh

    For those who are put off by the signature, my advance apologies for
    how the LORD has reshaped me:

    http://tinyurl.com/bgfqt

    Prayerfully in Christ's love,

    Andrew
    http://tinyurl.com/8juld
     
  17. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    >
    > > > > > > Whether inflammatory cytokines which are produced by visceral
    > > > > > > adipocytes is only reason to getting IR or all inflammatory responses
    > > > > > > can cause insulin resistance and hyperglycemia(infections are already
    > > > > > > indicated to increse blood glucose levels)?
    > > > > >
    > > > > > Chronically elevated levels of inflammatory cytokines likely has the
    > > > > > potential for causing IR regardless of the primary cause.
    > > > >
    > > > > Whether Chronically elevated levels of inflammatory cytokines can be
    > > > > the only/main cause of getting IR?
    > > >
    > > > It is the only cause we know of at the moment.

    > >
    > > Thanks. Iron imbalances and relaxed conditions of blood
    > > vessels(dilation) (may be swelling,acidosis,pain) look to be related to
    > > inflammatory diseases. How these conditions can be related to adiposity
    > > and getting inflammatory cytolines?

    >
    > You are mixing up acute with chronic conditions.


    Is there any relation between iron imbalance and IR/hyperglycemia?
    >
    > > > > > > As such, can greater adiposity or obesity be treated as inflammatory
    > > > > > > diseases?
    > > > > >
    > > > > > Far wiser would be to address the primary reason for the
    > > > > > adiposity/obesity.
    > > > >
    > > > > What is that? Is it taking excess glucose/fats?
    > > >
    > > > Overeating.
    > > >

    > > Can exposure of various foods, easy cooking, easy availabilty of foods,
    > > stress i.e. modern lifestyle in big cities and pollution can cause
    > > excess cravings and overeating?

    >
    > Healthy people have healthy appetites (hunger and cravings).
    >
    > Those who are afraid of hunger tend to overeat.
    >
    > Those who are not afraid of hunger are able to avoid overeating.
    >
    > The latter state of befriending hunger is an enlightened choice.
    >

    Who are afraid of hunger?

    ..
    >
    > > > > > > > > > > Will then
    > > > > > > > > > > insulin be normally effective to these new cells?
    > > > > > > > > >
    > > > > > > > > > Not in the setting of metabolic syndrome (MetS).
    > > > > > >
    > > > > > > Does it indicate that it is due to genetic predisposition?
    > > > > > >
    > > > > >
    > > > > > There is a genetic predisposition to develop MetS.
    > > > >
    > > > > Can genetic predisostions in diabetes2 basically cause excess cravings
    > > > > to foods resulting into more food intake>>more glucose>>more
    > > > > insulin>>IR>>hyperglycemia....?
    > > >
    > > > No. It lowers the threshold of amount of visceral adiposity before IR
    > > > occurs.
    > > >

    > > Yes but how?

    >
    > Through insulin receptor number, insulin binding affinity, baseline
    > levels of inflammatory cytokines, second messenger signalling pathways,
    > gene regulatory promoter elements, etc.
    >
    > > Whether visceral adiposity is a natural body response to
    > > protect organs in inflammatory conditions?

    >
    > No. Visceral adiposity is an unnatural condition arising from
    > overeating.
    >

    If insulin resistant patient left untreated for diabetic medications,
    can inflammatory cytokines/responses treat visceral adiposity?

    > > > > If yes, how this excess craving is oriented? Is it by genetic
    > > > > predisposition to get excess gastric acid and insulin secretion?
    > > >
    > > > No.
    > > >

    > >
    > > Or as above which I mentioned..modern lifestyle and atmosphere?

    >
    > No. Hunger is a healthy state.
    >

    What about craving in diabetic patients, eg; alcoholic patient's
    craving for alcohol?

    > > Btw, how getting diabetes2, IR and hypertentions are different in big
    > > polluted and crowded cities and in clean environment remote and natural
    > > areas of small villages or in jungles?

    >
    > No difference.
    >


    Many time diabetic patient(myself also) find that his persistent higher
    glucose in blood is well controlled inspite of taking excess food and
    similar activities on visiting some remote/green area. ??
    > > > > Can't aggregation/assotiation or concentration of insulin molecules by
    > > > > Hydrostatic and electrostatic intermolecular interactions AND by its
    > > > > oligomerization be a natural body mechanism to control/balance/maintain
    > > > > and store(either of these) insulin levels in blood--aggregation
    > > > > somewhat medium acting and oligomerization somewhat long acting?
    > > >
    > > > No. Again, storage of insulin would disrupt its signalling function.
    > > >

    > >
    > > Yes, but some insulin can be stored for prolonged requirements due to
    > > persitent hyperglycemia. This looks alike IR.

    >
    > No.
    >
    > > Btw, whether pacreas can continuously secrete insulin or need some time
    > > to refill--in normal health and in diabetes2?

    >
    > The former.
    >

    Thanks.
    > >
    > > > > >Again, insulin is
    > > > > > catabolized by the kidneys and not excreted.
    > > > >
    > > > > Does it mean that it is filtered and lost its origional form as
    > > > > degraded/denatured in kidneys(in loosing i am not counting reabsorption
    > > > > of degraded/denatured form)? Or, it is degraded/denatured at other
    > > > > parts(say liver) and filtered and lost in its degraded/denatured form?
    > > >
    > > > It simply is not excreted but catabolized.
    > > >

    > > Ok, it looks like suspense. Cells uses insulin in kidney's area is a
    > > different aspect but whether some insulin in reasonable quantity
    > > effecting glucose levels in blood is lost via kidneys or not in normal
    > > health or in some disease?

    >
    > There is no excretion of insulin by the kidneys. Intact insulin
    > polypeptide molecules are not present in the urine in significant
    > amounts in normal people.
    >

    What about insulin is lost in urine in degraded or deformed form(not
    intact) effected by more acidic/alkaline environment as present in
    kidneys/bladder? I mean insulin is filtered intact but lost its intact
    form in urine so not traced in urine?
    > > Yes, thanks. Is there any medicine which can directly control these
    > > inflammatory cytokines without controlling adiposity?

    >
    > No.
    >
    > > NSAIDs??

    >
    > No.
    >
    > Why look for medicine when permanent weight loss cures this?
    >
    > http://www.HeartMDPhD.com/wtloss.asp


    Thanks.

    Btw, can insulin cause hypertention, low HDL, high trigycerides in
    blood--- due to its effect on fats depositions?
     
  18. Kumar wrote:
    > Andrew B. Chung, MD/PhD wrote:
    > > Kumar wrote:
    > >
    > > > > > > > Whether inflammatory cytokines which are produced by visceral
    > > > > > > > adipocytes is only reason to getting IR or all inflammatory responses
    > > > > > > > can cause insulin resistance and hyperglycemia(infections are already
    > > > > > > > indicated to increse blood glucose levels)?
    > > > > > >
    > > > > > > Chronically elevated levels of inflammatory cytokines likely has the
    > > > > > > potential for causing IR regardless of the primary cause.
    > > > > >
    > > > > > Whether Chronically elevated levels of inflammatory cytokines can be
    > > > > > the only/main cause of getting IR?
    > > > >
    > > > > It is the only cause we know of at the moment.
    > > >
    > > > Thanks. Iron imbalances and relaxed conditions of blood
    > > > vessels(dilation) (may be swelling,acidosis,pain) look to be related to
    > > > inflammatory diseases. How these conditions can be related to adiposity
    > > > and getting inflammatory cytolines?

    > >
    > > You are mixing up acute with chronic conditions.

    >
    > Is there any relation between iron imbalance and IR/hyperglycemia?


    Iron overload can cause beta islet cell loss.

    > > > > > > > As such, can greater adiposity or obesity be treated as inflammatory
    > > > > > > > diseases?
    > > > > > >
    > > > > > > Far wiser would be to address the primary reason for the
    > > > > > > adiposity/obesity.
    > > > > >
    > > > > > What is that? Is it taking excess glucose/fats?
    > > > >
    > > > > Overeating.
    > > > >
    > > > Can exposure of various foods, easy cooking, easy availabilty of foods,
    > > > stress i.e. modern lifestyle in big cities and pollution can cause
    > > > excess cravings and overeating?

    > >
    > > Healthy people have healthy appetites (hunger and cravings).
    > >
    > > Those who are afraid of hunger tend to overeat.
    > >
    > > Those who are not afraid of hunger are able to avoid overeating.
    > >
    > > The latter state of befriending hunger is an enlightened choice.

    >
    > Who are afraid of hunger?


    Many are without being aware of it.

    > > > > > > > > > > > Will then
    > > > > > > > > > > > insulin be normally effective to these new cells?
    > > > > > > > > > >
    > > > > > > > > > > Not in the setting of metabolic syndrome (MetS).
    > > > > > > >
    > > > > > > > Does it indicate that it is due to genetic predisposition?
    > > > > > > >
    > > > > > >
    > > > > > > There is a genetic predisposition to develop MetS.
    > > > > >
    > > > > > Can genetic predisostions in diabetes2 basically cause excess cravings
    > > > > > to foods resulting into more food intake>>more glucose>>more
    > > > > > insulin>>IR>>hyperglycemia....?
    > > > >
    > > > > No. It lowers the threshold of amount of visceral adiposity before IR
    > > > > occurs.
    > > > >
    > > > Yes but how?

    > >
    > > Through insulin receptor number, insulin binding affinity, baseline
    > > levels of inflammatory cytokines, second messenger signalling pathways,
    > > gene regulatory promoter elements, etc.
    > >
    > > > Whether visceral adiposity is a natural body response to
    > > > protect organs in inflammatory conditions?

    > >
    > > No. Visceral adiposity is an unnatural condition arising from
    > > overeating.

    >
    > If insulin resistant patient left untreated for diabetic medications,
    > can inflammatory cytokines/responses treat visceral adiposity?


    No. Only eating less reduces visceral adiposity.

    > > > > > If yes, how this excess craving is oriented? Is it by genetic
    > > > > > predisposition to get excess gastric acid and insulin secretion?
    > > > >
    > > > > No.
    > > > >
    > > >
    > > > Or as above which I mentioned..modern lifestyle and atmosphere?

    > >
    > > No. Hunger is a healthy state.

    >
    > What about craving in diabetic patients, eg; alcoholic patient's
    > craving for alcohol?


    Craving is a healthy state. Fear of the craving is what leads to
    worsening diabetes and worsening alcoholism.

    > > > Btw, how getting diabetes2, IR and hypertentions are different in big
    > > > polluted and crowded cities and in clean environment remote and natural
    > > > areas of small villages or in jungles?

    > >
    > > No difference.
    > >

    >
    > Many time diabetic patient(myself also) find that his persistent higher
    > glucose in blood is well controlled inspite of taking excess food and
    > similar activities on visiting some remote/green area. ??


    Estimates of amount of food ingested are not reliable especially for
    folks who are in stressful environments (crowds, hustle and bustle)
    which tend to increase hunger.

    > > > > > Can't aggregation/assotiation or concentration of insulin molecules by
    > > > > > Hydrostatic and electrostatic intermolecular interactions AND by its
    > > > > > oligomerization be a natural body mechanism to control/balance/maintain
    > > > > > and store(either of these) insulin levels in blood--aggregation
    > > > > > somewhat medium acting and oligomerization somewhat long acting?
    > > > >
    > > > > No. Again, storage of insulin would disrupt its signalling function.
    > > > >
    > > >
    > > > Yes, but some insulin can be stored for prolonged requirements due to
    > > > persitent hyperglycemia. This looks alike IR.

    > >
    > > No.
    > >
    > > > Btw, whether pacreas can continuously secrete insulin or need some time
    > > > to refill--in normal health and in diabetes2?

    > >
    > > The former.
    > >

    > Thanks.
    > > >
    > > > > > >Again, insulin is
    > > > > > > catabolized by the kidneys and not excreted.
    > > > > >
    > > > > > Does it mean that it is filtered and lost its origional form as
    > > > > > degraded/denatured in kidneys(in loosing i am not counting reabsorption
    > > > > > of degraded/denatured form)? Or, it is degraded/denatured at other
    > > > > > parts(say liver) and filtered and lost in its degraded/denatured form?
    > > > >
    > > > > It simply is not excreted but catabolized.
    > > > >
    > > > Ok, it looks like suspense. Cells uses insulin in kidney's area is a
    > > > different aspect but whether some insulin in reasonable quantity
    > > > effecting glucose levels in blood is lost via kidneys or not in normal
    > > > health or in some disease?

    > >
    > > There is no excretion of insulin by the kidneys. Intact insulin
    > > polypeptide molecules are not present in the urine in significant
    > > amounts in normal people.
    > >

    > What about insulin is lost in urine in degraded or deformed form(not
    > intact) effected by more acidic/alkaline environment as present in
    > kidneys/bladder? I mean insulin is filtered intact but lost its intact
    > form in urine so not traced in urine?


    There are no proteases in urine that would degrade insulin.

    > > > Yes, thanks. Is there any medicine which can directly control these
    > > > inflammatory cytokines without controlling adiposity?

    > >
    > > No.
    > >
    > > > NSAIDs??

    > >
    > > No.
    > >
    > > Why look for medicine when permanent weight loss cures this?
    > >
    > > http://www.HeartMDPhD.com/wtloss.asp

    >
    > Thanks.


    You are welcome :)

    > Btw, can insulin cause hypertention, low HDL, high trigycerides in
    > blood--- due to its effect on fats depositions?


    If it could, everyone would have hypertension, low HDL, and high
    triglycerides except type I diabetics **before** insulin therapy.

    Will be available to "glow" and chat about this and other things like
    cardiology, diabetes, cooking and nutrition that interest those
    following this thread here during the next on-line chat (02/02/06) from
    6 to 7 pm EST:

    http://tinyurl.com/cpayh

    For those who are put off by the signature, my advance apologies for
    how the LORD has reshaped me:

    http://tinyurl.com/bgfqt

    Prayerfully in Christ's love,

    Andrew
    http://tinyurl.com/8juld
     
  19. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > Andrew B. Chung, MD/PhD wrote:
    > > > Kumar wrote:
    > > >
    > > > > > > > > Whether inflammatory cytokines which are produced by visceral
    > > > > > > > > adipocytes is only reason to getting IR or all inflammatory responses
    > > > > > > > > can cause insulin resistance and hyperglycemia(infections are already
    > > > > > > > > indicated to increse blood glucose levels)?
    > > > > > > >
    > > > > > > > Chronically elevated levels of inflammatory cytokines likely has the
    > > > > > > > potential for causing IR regardless of the primary cause.
    > > > > > >
    > > > > > > Whether Chronically elevated levels of inflammatory cytokines can be
    > > > > > > the only/main cause of getting IR?
    > > > > >
    > > > > > It is the only cause we know of at the moment.
    > > > >
    > > > > Thanks. Iron imbalances and relaxed conditions of blood
    > > > > vessels(dilation) (may be swelling,acidosis,pain) look to be related to
    > > > > inflammatory diseases. How these conditions can be related to adiposity
    > > > > and getting inflammatory cytolines?
    > > >
    > > > You are mixing up acute with chronic conditions.

    > >
    > > Is there any relation between iron imbalance and IR/hyperglycemia?

    >
    > Iron overload can cause beta islet cell loss.
    >

    Whether excess gastric acid secretion is related to iron overload due
    to better digestion of iron containing foods(other than non-veg/iron
    supplements) so better absorption? Can excess acid cause overriding of
    intestinal mucus lining resulting into more iron absorption??
    > > > > > > > > As such, can greater adiposity or obesity be treated as inflammatory
    > > > > > > > > diseases?
    > > > > > > >
    > > > > > > > Far wiser would be to address the primary reason for the
    > > > > > > > adiposity/obesity.
    > > > > > >
    > > > > > > What is that? Is it taking excess glucose/fats?
    > > > > >
    > > > > > Overeating.
    > > > > >
    > > > > Can exposure of various foods, easy cooking, easy availabilty of foods,
    > > > > stress i.e. modern lifestyle in big cities and pollution can cause
    > > > > excess cravings and overeating?
    > > >
    > > > Healthy people have healthy appetites (hunger and cravings).
    > > >
    > > > Those who are afraid of hunger tend to overeat.
    > > >
    > > > Those who are not afraid of hunger are able to avoid overeating.
    > > >
    > > > The latter state of befriending hunger is an enlightened choice.

    > >
    > > Who are afraid of hunger?

    >
    > Many are without being aware of it.
    >

    It is due to more insulin secretion(probably more gastric acid
    secretion also) in diabetic2 patients?
    > > > > > > > > > > > > Will then
    > > > > > > > > > > > > insulin be normally effective to these new cells?
    > > > > > > > > > > >
    > > > > > > > > > > > Not in the setting of metabolic syndrome (MetS).
    > > > > > > > >
    > > > > > > > > Does it indicate that it is due to genetic predisposition?
    > > > > > > > >
    > > > > > > >
    > > > > > > > There is a genetic predisposition to develop MetS.
    > > > > > >
    > > > > > > Can genetic predisostions in diabetes2 basically cause excess cravings
    > > > > > > to foods resulting into more food intake>>more glucose>>more
    > > > > > > insulin>>IR>>hyperglycemia....?
    > > > > >
    > > > > > No. It lowers the threshold of amount of visceral adiposity before IR
    > > > > > occurs.
    > > > > >
    > > > > Yes but how?
    > > >
    > > > Through insulin receptor number, insulin binding affinity, baseline
    > > > levels of inflammatory cytokines, second messenger signalling pathways,
    > > > gene regulatory promoter elements, etc.
    > > >
    > > > > Whether visceral adiposity is a natural body response to
    > > > > protect organs in inflammatory conditions?
    > > >
    > > > No. Visceral adiposity is an unnatural condition arising from
    > > > overeating.

    > >
    > > If insulin resistant patient left untreated for diabetic medications,
    > > can inflammatory cytokines/responses treat visceral adiposity?

    >
    > No. Only eating less reduces visceral adiposity.
    >

    Can eating more carbs(not fats) be only relared to getting greater
    visceral adiposity?
    Do we have insulin resistance to fat stores--may be by producing more
    adipokines (the cytokines produced by adipose tissue)? Why body opt to
    getting visceral adiposity instead of subcutnous?

    > > > > > > If yes, how this excess craving is oriented? Is it by genetic
    > > > > > > predisposition to get excess gastric acid and insulin secretion?
    > > > > >
    > > > > > No.
    > > > > >
    > > > >
    > > > > Or as above which I mentioned..modern lifestyle and atmosphere?
    > > >
    > > > No. Hunger is a healthy state.

    > >
    > > What about craving in diabetic patients, eg; alcoholic patient's
    > > craving for alcohol?

    >
    > Craving is a healthy state. Fear of the craving is what leads to
    > worsening diabetes and worsening alcoholism.
    >

    I really don't follow "fear of craving or fear of hunger". Is it due to
    cells not getting enough glucose?

    > > > > Btw, how getting diabetes2, IR and hypertentions are different in big
    > > > > polluted and crowded cities and in clean environment remote and natural
    > > > > areas of small villages or in jungles?
    > > >
    > > > No difference.
    > > >

    > >
    > > Many time diabetic patient(myself also) find that his persistent higher
    > > glucose in blood is well controlled inspite of taking excess food and
    > > similar activities on visiting some remote/green area. ??

    >
    > Estimates of amount of food ingested are not reliable especially for
    > folks who are in stressful environments (crowds, hustle and bustle)
    > which tend to increase hunger.
    >

    How it tends to increase hunger?

    > > > > > > Can't aggregation/assotiation or concentration of insulin molecules by
    > > > > > > Hydrostatic and electrostatic intermolecular interactions AND by its
    > > > > > > oligomerization be a natural body mechanism to control/balance/maintain
    > > > > > > and store(either of these) insulin levels in blood--aggregation
    > > > > > > somewhat medium acting and oligomerization somewhat long acting?
    > > > > >
    > > > > > No. Again, storage of insulin would disrupt its signalling function.
    > > > > >
    > > > >
    > > > > Yes, but some insulin can be stored for prolonged requirements due to
    > > > > persitent hyperglycemia. This looks alike IR.
    > > >
    > > > No.
    > > >
    > > > > Btw, whether pacreas can continuously secrete insulin or need some time
    > > > > to refill--in normal health and in diabetes2?
    > > >
    > > > The former.
    > > >

    > > Thanks.
    > > > >
    > > > > > > >Again, insulin is
    > > > > > > > catabolized by the kidneys and not excreted.
    > > > > > >
    > > > > > > Does it mean that it is filtered and lost its origional form as
    > > > > > > degraded/denatured in kidneys(in loosing i am not counting reabsorption
    > > > > > > of degraded/denatured form)? Or, it is degraded/denatured at other
    > > > > > > parts(say liver) and filtered and lost in its degraded/denatured form?
    > > > > >
    > > > > > It simply is not excreted but catabolized.
    > > > > >
    > > > > Ok, it looks like suspense. Cells uses insulin in kidney's area is a
    > > > > different aspect but whether some insulin in reasonable quantity
    > > > > effecting glucose levels in blood is lost via kidneys or not in normal
    > > > > health or in some disease?
    > > >
    > > > There is no excretion of insulin by the kidneys. Intact insulin
    > > > polypeptide molecules are not present in the urine in significant
    > > > amounts in normal people.
    > > >

    > > What about insulin is lost in urine in degraded or deformed form(not
    > > intact) effected by more acidic/alkaline environment as present in
    > > kidneys/bladder? I mean insulin is filtered intact but lost its intact
    > > form in urine so not traced in urine?

    >
    > There are no proteases in urine that would degrade insulin.
    >

    Thanks.
    > > Btw, can insulin cause hypertention, low HDL, high trigycerides in
    > > blood--- due to its effect on fats depositions?

    >
    > If it could, everyone would have hypertension, low HDL, and high
    > triglycerides except type I diabetics **before** insulin therapy.
    >

    Yes but can't more insulin--medicated or natural which is not used in
    IR cases, cause it?

    "Various disease states make the body tissues more resistant to the
    actions of insulin. Example include infection (TNFa) and **acidosis**.
    Recent research involves the relative roles of adipokines (the
    cytokines produced by adipose tissue) in modifying insulin resistance.
    http://en.wikipedia.org/wiki/Insulin_resistance "

    This link suggest acidosis as one cause for insulin resistance. Is it
    right? If yes, how it happens?
     
  20. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > > What about insulin is lost in urine in degraded or deformed form(not
    > > intact) effected by more acidic/alkaline environment as present in
    > > kidneys/bladder? I mean insulin is filtered intact but lost its intact
    > > form in urine so not traced in urine?

    >
    > There are no proteases in urine that would degrade insulin.
    >


    Continuance to last post....

    Can it happen in following indicated manner:-

    "The resulting highly acidic environment in the stomach lumen causes
    proteins from food to lose their characteristic folded structure (or
    denature). This exposes the protein's peptide bonds.
    http://en.wikipedia.org/wiki/Gastric_acid "

    Moreover can't fate of proteases in urine be alike of insulin or these
    are reabsorbed so not traced in intact form?
     
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