Re: Fatty Liver

Discussion in 'Food and nutrition' started by Andrew B. Chung, MD/PhD, Jan 22, 2006.

  1. Kumar wrote:
    > Pls look at following hypothesis:-
    >
    > Ectopic Fat Storage Syndrome
    >
    > The ectopic fat storage syndrome hypothesis suggests that as adipocytes
    > hypertrophy and reach their capacity for storing more fat, then
    > additional fat from excess dietary lipids or calories is deferred to
    > non-adipose tissues intracellularly, e.g. liver, skeletal muscle,
    > heart, and the beta cells of the pancreas where they can exert toxic
    > effects and dysfunction . This "lipotoxicity" may also be exacerbated
    > by impaired oxidation of fat within tissues . Furthermore, adipose
    > tissue is a major endocrine organ that secretes numerous polypeptide
    > hormones and cytokines that are proinflammatory and proatherogenic.
    > These play a major role in affecting insulin action in skeletal muscle
    > and creating a low-grade state of inflammation and endothelial
    > dysfunction . Compared to SCAT, VAT has been correlated more with
    > endothelial dysfunction .
    >
    > CVATT-A Working Hypothesis
    >
    > It must be emphasized that the current proposal is a working
    > hypothesis. Figure 1 describes a critical VAT threshold (CVATT) which
    > is unique for a given individual and represents a range for the
    > accumulation of a critical mass of VAT (CVATT) that when achieved,
    > leads to the development of metabolic syndrome. Note that insulin
    > sensitivity is important for weight gain and accumulation of VAT, and
    > investigators have proposed that insulin resistance may actually, to a
    > certain extent, be beneficial by protecting cells with already impaired
    > fatty acid oxidation. Once the CVATT is reached, insulin resistance
    > (IR) occurs, which may be protective initially . In addition to
    > protecting against further weight and fat gain , insulin resistance
    > prevents glucose and more fat from entering the cell and becoming
    > preferentially oxidized. Hence, insulin resistance also allows
    > intracellular fat already present within the cell to become oxidized
    > rather than cause further damage through "lipotoxicity ."
    > http://www.diabetesincontrol.com/modules.php?name=News&file=article&sid=2260
    > "
    >
    > The above link indicate many aspects. It tells about possibility of
    > fats resistance in adipocytes resulting into their diversion to other
    > vital parts Can you comment on it?


    This is metabolic syndrome (MetS).

    Would be more than happy 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 (01/26/06) 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/be9va
     
    Tags:


  2. Andrew B. Chung, MD/PhD wrote:

    > For those who are put off by the signature, my advance apologies for
    > how the LORD has reshaped me:
    >
    > Prayerfully in Christ's love,


    ~ A History of the Mind-Body Connection ~
    http://naturalhealthperspective.com/tutorials/history-mind-body-connection.html
    "1940s>{Wellness}During the 1940s the self-help movement became
    increasingly more psychologically oriented and was devoid of religious
    overtones.[9]"

    Andrew strikes me as one deeply confused puppy. :(

    You seem to be unable to make up your mind whether good health is a
    result of lifestyle, praying, or faith healing. :(

    Thus, your confused muddy contradictory advice is very likely to induce
    Neurasthenia in your targeted audience. :(

    Confused puppies, such as yourself, really need to make up your mind
    which works better: Praying or Changing Lifestyle factors. Make up
    your mind Andrew, and STOP trying to confuse the hell out of the
    public.

    Just thought that you might want to know.
    --
    john gohde
    Please read my tutorials Andrew. You need help, fast!
    http://naturalhealthperspective.com/tutorials/
     
  3. Kumar

    Kumar Guest

    Reply against my post no 34 is pending.

    Can you tell something about this mentioning in below quoted post:-

    "Furthermore, adipose
    tissue is a major endocrine organ that secretes numerous polypeptide
    hormones and cytokines that are proinflammatory and proatherogenic."

    Does it the property of only adipose tisse or also of other tissues?


    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > Pls look at following hypothesis:-
    > >
    > > Ectopic Fat Storage Syndrome
    > >
    > > The ectopic fat storage syndrome hypothesis suggests that as adipocytes
    > > hypertrophy and reach their capacity for storing more fat, then
    > > additional fat from excess dietary lipids or calories is deferred to
    > > non-adipose tissues intracellularly, e.g. liver, skeletal muscle,
    > > heart, and the beta cells of the pancreas where they can exert toxic
    > > effects and dysfunction . This "lipotoxicity" may also be exacerbated
    > > by impaired oxidation of fat within tissues . Furthermore, adipose
    > > tissue is a major endocrine organ that secretes numerous polypeptide
    > > hormones and cytokines that are proinflammatory and proatherogenic.
    > > These play a major role in affecting insulin action in skeletal muscle
    > > and creating a low-grade state of inflammation and endothelial
    > > dysfunction . Compared to SCAT, VAT has been correlated more with
    > > endothelial dysfunction .
    > >
    > > CVATT-A Working Hypothesis
    > >
    > > It must be emphasized that the current proposal is a working
    > > hypothesis. Figure 1 describes a critical VAT threshold (CVATT) which
    > > is unique for a given individual and represents a range for the
    > > accumulation of a critical mass of VAT (CVATT) that when achieved,
    > > leads to the development of metabolic syndrome. Note that insulin
    > > sensitivity is important for weight gain and accumulation of VAT, and
    > > investigators have proposed that insulin resistance may actually, to a
    > > certain extent, be beneficial by protecting cells with already impaired
    > > fatty acid oxidation. Once the CVATT is reached, insulin resistance
    > > (IR) occurs, which may be protective initially . In addition to
    > > protecting against further weight and fat gain , insulin resistance
    > > prevents glucose and more fat from entering the cell and becoming
    > > preferentially oxidized. Hence, insulin resistance also allows
    > > intracellular fat already present within the cell to become oxidized
    > > rather than cause further damage through "lipotoxicity ."
    > > http://www.diabetesincontrol.com/modules.php?name=News&file=article&sid=2260
    > > "
    > >
    > > The above link indicate many aspects. It tells about possibility of
    > > fats resistance in adipocytes resulting into their diversion to other
    > > vital parts Can you comment on it?

    >
    > This is metabolic syndrome (MetS).
    >
    > Would be more than happy 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 (01/26/06) 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/be9va
     
  4. Kumar wrote:
    > Reply against my post no 34 is pending.
    >
    > Can you tell something about this mentioning in below quoted post:-
    >
    > "Furthermore, adipose
    > tissue is a major endocrine organ that secretes numerous polypeptide
    > hormones and cytokines that are proinflammatory and proatherogenic."
    >
    > Does it the property of only adipose tisse or also of other tissues?


    Just the visceral adipocytes.

    Would be more than happy 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 (01/26/06) 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/be9va
     
  5. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > Reply against my post no 34 is pending.
    > >
    > > Can you tell something about this mentioning in below quoted post:-
    > >
    > > "Furthermore, adipose
    > > tissue is a major endocrine organ that secretes numerous polypeptide
    > > hormones and cytokines that are proinflammatory and proatherogenic."
    > >
    > > Does it the property of only adipose tisse or also of other tissues?

    >
    > Just the visceral adipocytes.


    Pls reply my post no 34.

    "Furthermore, adipose
    tissue is a major endocrine organ that secretes numerous polypeptide
    hormones and cytokines that are proinflammatory and proatherogenic."

    Do excess fats in tissues is proinflamatory, proatherogenic,
    prodiabetic, proacidosis, procanerous?
     
  6. Kumar wrote:
    > Andrew B. Chung, MD/PhD wrote:
    > > Kumar wrote:
    > > > Reply against my post no 34 is pending.
    > > >
    > > > Can you tell something about this mentioning in below quoted post:-
    > > >
    > > > "Furthermore, adipose
    > > > tissue is a major endocrine organ that secretes numerous polypeptide
    > > > hormones and cytokines that are proinflammatory and proatherogenic."
    > > >
    > > > Does it the property of only adipose tisse or also of other tissues?

    > >
    > > Just the visceral adipocytes.

    >
    > Pls reply my post no 34.


    Post#34 in this thread in the Google archive is from me.

    > "Furthermore, adipose
    > tissue is a major endocrine organ that secretes numerous polypeptide
    > hormones and cytokines that are proinflammatory and proatherogenic."
    >
    > Do excess fats in tissues is proinflamatory, proatherogenic,
    > prodiabetic, proacidosis, procanerous?


    Yes to all the above except for "proacidosis."

    Would be more than happy 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 (01/26/06) 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/cbn2r
     
  7. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > Reply against my post no 34 is pending.


    When I sort by date it comes 34 as under;

    34. Kumar
    Jan 22, 11:57 am show options

    Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
    From: "Kumar" <[email protected]> - Find messages by this
    author
    Date: 21 Jan 2006 22:57:57 -0800
    Local: Sun, Jan 22 2006 11:57 am
    Subject: Re: Fatty Liver
    Reply | Reply to Author | Forward | Print | Individual Message | Show
    original | Remove | Report Abuse


    Andrew B. Chung, MD/PhD wrote:



    > Kumar wrote:


    > > > The longer half-life of insulin is due to decreased rates of
    > > > degradation and not decreased rates of excretion.



    > > > and so he may need to adjust injected insulin



    > > Can you explain how decreased rates of degradation of insulin happen?



    > Loss of nephrons where the degradation occurs.




    Whether loss of nephrons causes increased or decreased filteration? On
    one hand we say lesser filteration on other hand protiens(bigger
    molecules) start coming into urine on getting DN?


    > > What about cluster or crystal formation possibilty of molecules of
    > > insulin?


    > There is no reason to invoke this.



    > > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
    > > > > stages?



    > > > Insulin is not excreted in the urine.



    > > Why when the molecyular weight of insulin is more than 1/4th of
    > > filteration capacity of kydneys?



    > You just answered your question by your question.




    Sorry, I meant; Why insulin is not filtered in kidneys, when the
    molecular weight of insulin is less than 1/4th (less than 6000 D) of
    filteration capacity of kidneys (30000 D)?


    > > Moreover capillary permeability for
    > > insulin is considered as 0.2.


    > The glomeruli of nephrons of the kidney are considerably less permeable
    > to polypeptides such as insulin than capillary beds.




    Can it mean that extra cellular fluids in our tissues will have bigger
    molecules than as we have in urine alike insulin?
    >
     
  8. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:

    ..
    >
    > > "Furthermore, adipose
    > > tissue is a major endocrine organ that secretes numerous polypeptide
    > > hormones and cytokines that are proinflammatory and proatherogenic."
    > >
    > > Do excess fats in tissues is proinflamatory, proatherogenic,
    > > prodiabetic, proacidosis, procanerous?

    >
    > Yes to all the above except for "proacidosis."


    Can it(VApro-alkaliosis and pro-azoospermia?
    Whether inflammatory, atherogenic,cancerous, diabetic effects are
    pro-acidosis or pro-alkaliosis?
     
  9. Kumar wrote:
    > Andrew B. Chung, MD/PhD wrote:
    > > Kumar wrote:
    > > > Reply against my post no 34 is pending.

    >
    > When I sort by date it comes 34 as under;
    >
    > 34. Kumar
    > Jan 22, 11:57 am show options
    >
    > Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
    > From: "Kumar" <[email protected]> - Find messages by this
    > author
    > Date: 21 Jan 2006 22:57:57 -0800
    > Local: Sun, Jan 22 2006 11:57 am
    > Subject: Re: Fatty Liver
    > Reply | Reply to Author | Forward | Print | Individual Message | Show
    > original | Remove | Report Abuse
    >
    > Andrew B. Chung, MD/PhD wrote:
    >
    > > Kumar wrote:

    >
    > > > > The longer half-life of insulin is due to decreased rates of
    > > > > degradation and not decreased rates of excretion.

    >
    >
    > > > > and so he may need to adjust injected insulin

    >
    >
    > > > Can you explain how decreased rates of degradation of insulin happen?

    >
    >
    > > Loss of nephrons where the degradation occurs.

    >
    >
    >
    > Whether loss of nephrons causes increased or decreased filteration?


    Decreased

    > On
    > one hand we say lesser filteration on other hand protiens(bigger
    > molecules) start coming into urine on getting DN?


    Proteinuria does happen with DN but this does not appreciably alter the
    half-life of insulin.

    > > > What about cluster or crystal formation possibilty of molecules of
    > > > insulin?

    >
    > > There is no reason to invoke this.

    >
    >
    > > > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
    > > > > > stages?

    >
    >
    > > > > Insulin is not excreted in the urine.

    >
    >
    > > > Why when the molecyular weight of insulin is more than 1/4th of
    > > > filteration capacity of kydneys?

    >
    >
    > > You just answered your question by your question.

    >
    > Sorry, I meant; Why insulin is not filtered in kidneys, when the
    > molecular weight of insulin is less than 1/4th (less than 6000 D) of
    > filteration capacity of kidneys (30000 D)?


    Insulin is a charged polypeptide that will not get through the
    glomerular basement membrane which is a more effective barrier when a
    macromolecule has a charge.

    > > > Moreover capillary permeability for
    > > > insulin is considered as 0.2.

    >
    > > The glomeruli of nephrons of the kidney are considerably less permeable
    > > to polypeptides such as insulin than capillary beds.

    >
    > Can it mean that extra cellular fluids in our tissues will have bigger
    > molecules than as we have in urine alike insulin?


    Yes.

    Would be more than happy 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 (01/26/06) 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/cbn2r
     
  10. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > Andrew B. Chung, MD/PhD wrote:
    > > > Kumar wrote:
    > > > > Reply against my post no 34 is pending.

    > >
    > > When I sort by date it comes 34 as under;
    > >
    > > 34. Kumar
    > > Jan 22, 11:57 am show options
    > >
    > > Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
    > > From: "Kumar" <[email protected]> - Find messages by this
    > > author
    > > Date: 21 Jan 2006 22:57:57 -0800
    > > Local: Sun, Jan 22 2006 11:57 am
    > > Subject: Re: Fatty Liver
    > > Reply | Reply to Author | Forward | Print | Individual Message | Show
    > > original | Remove | Report Abuse
    > >
    > > Andrew B. Chung, MD/PhD wrote:
    > >
    > > > Kumar wrote:

    > >
    > > > > > The longer half-life of insulin is due to decreased rates of
    > > > > > degradation and not decreased rates of excretion.

    > >
    > >
    > > > > > and so he may need to adjust injected insulin

    > >
    > >
    > > > > Can you explain how decreased rates of degradation of insulin happen?

    > >
    > >
    > > > Loss of nephrons where the degradation occurs.

    > >
    > >
    > >
    > > Whether loss of nephrons causes increased or decreased filteration?

    >
    > Decreased
    >
    > > On
    > > one hand we say lesser filteration on other hand protiens(bigger
    > > molecules) start coming into urine on getting DN?

    >
    > Proteinuria does happen with DN but this does not appreciably alter the
    > half-life of insulin.


    I was just comparing the size of molecules with filteration as protiens
    are filtered but not insulin on getting DN.??

    > > > > What about cluster or crystal formation possibilty of molecules of
    > > > > insulin?

    > >
    > > > There is no reason to invoke this.

    > >
    > >
    > > > > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
    > > > > > > stages?

    > >
    > >
    > > > > > Insulin is not excreted in the urine.

    > >
    > >
    > > > > Why when the molecyular weight of insulin is more than 1/4th of
    > > > > filteration capacity of kydneys?

    > >
    > >
    > > > You just answered your question by your question.

    > >
    > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
    > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
    > > filteration capacity of kidneys (30000 D)?

    >
    > Insulin is a charged polypeptide that will not get through the
    > glomerular basement membrane which is a more effective barrier when a
    > macromolecule has a charge.


    Sorry, it is not clear to me.

    > > > > Moreover capillary permeability for
    > > > > insulin is considered as 0.2.

    > >
    > > > The glomeruli of nephrons of the kidney are considerably less permeable
    > > > to polypeptides such as insulin than capillary beds.

    > >
    > > Can it mean that extra cellular fluids in our tissues will have bigger
    > > molecules than as we have in urine alike insulin?

    >
    > Yes.


    Sorry following question is pending;

    > Yes to all the above except for "proacidosis."




    Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?

    Whether inflammatory, atherogenic,cancerous, diabetic effects are
    pro-acidosis or pro-alkaliosis?
     
  11. Kumar wrote:
    > Andrew B. Chung, MD/PhD wrote:
    > > Kumar wrote:
    > > > Andrew B. Chung, MD/PhD wrote:
    > > > > Kumar wrote:
    > > > > > Reply against my post no 34 is pending.
    > > >
    > > > When I sort by date it comes 34 as under;
    > > >
    > > > 34. Kumar
    > > > Jan 22, 11:57 am show options
    > > >
    > > > Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
    > > > From: "Kumar" <[email protected]> - Find messages by this
    > > > author
    > > > Date: 21 Jan 2006 22:57:57 -0800
    > > > Local: Sun, Jan 22 2006 11:57 am
    > > > Subject: Re: Fatty Liver
    > > > Reply | Reply to Author | Forward | Print | Individual Message | Show
    > > > original | Remove | Report Abuse
    > > >
    > > > Andrew B. Chung, MD/PhD wrote:
    > > >
    > > > > Kumar wrote:
    > > >
    > > > > > > The longer half-life of insulin is due to decreased rates of
    > > > > > > degradation and not decreased rates of excretion.
    > > >
    > > >
    > > > > > > and so he may need to adjust injected insulin
    > > >
    > > >
    > > > > > Can you explain how decreased rates of degradation of insulin happen?
    > > >
    > > >
    > > > > Loss of nephrons where the degradation occurs.
    > > >
    > > >
    > > >
    > > > Whether loss of nephrons causes increased or decreased filteration?

    > >
    > > Decreased
    > >
    > > > On
    > > > one hand we say lesser filteration on other hand protiens(bigger
    > > > molecules) start coming into urine on getting DN?

    > >
    > > Proteinuria does happen with DN but this does not appreciably alter the
    > > half-life of insulin.

    >
    > I was just comparing the size of molecules with filteration as protiens
    > are filtered but not insulin on getting DN.??


    Depends on the protein.

    > > > > > What about cluster or crystal formation possibilty of molecules of
    > > > > > insulin?
    > > >
    > > > > There is no reason to invoke this.
    > > >
    > > >
    > > > > > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
    > > > > > > > stages?
    > > >
    > > >
    > > > > > > Insulin is not excreted in the urine.
    > > >
    > > >
    > > > > > Why when the molecyular weight of insulin is more than 1/4th of
    > > > > > filteration capacity of kydneys?
    > > >
    > > >
    > > > > You just answered your question by your question.
    > > >
    > > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
    > > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
    > > > filteration capacity of kidneys (30000 D)?

    > >
    > > Insulin is a charged polypeptide that will not get through the
    > > glomerular basement membrane which is a more effective barrier when a
    > > macromolecule has a charge.

    >
    > Sorry, it is not clear to me.


    The glomerular basement membrane is **selectively** permeable.

    > > > > > Moreover capillary permeability for
    > > > > > insulin is considered as 0.2.
    > > >
    > > > > The glomeruli of nephrons of the kidney are considerably less permeable
    > > > > to polypeptides such as insulin than capillary beds.
    > > >
    > > > Can it mean that extra cellular fluids in our tissues will have bigger
    > > > molecules than as we have in urine alike insulin?

    > >
    > > Yes.

    >
    > Sorry following question is pending;
    >
    > > Yes to all the above except for "proacidosis."

    >
    > Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?


    VA ?

    > Whether inflammatory, atherogenic,cancerous, diabetic effects are
    > pro-acidosis or pro-alkaliosis?


    The buffering capacity of serum bicarbonate with normal pulmonary
    function is such that serum pH is well regulated even in the face of
    most metabolic derangements.

    Would be more than happy 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 (01/26/06) 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/cbn2r
     
  12. 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:
    > > > > > > Reply against my post no 34 is pending.
    > > > >
    > > > > When I sort by date it comes 34 as under;
    > > > >
    > > > > 34. Kumar
    > > > > Jan 22, 11:57 am show options
    > > > >
    > > > > Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
    > > > > From: "Kumar" <[email protected]> - Find messages by this
    > > > > author
    > > > > Date: 21 Jan 2006 22:57:57 -0800
    > > > > Local: Sun, Jan 22 2006 11:57 am
    > > > > Subject: Re: Fatty Liver
    > > > > Reply | Reply to Author | Forward | Print | Individual Message | Show
    > > > > original | Remove | Report Abuse
    > > > >
    > > > > Andrew B. Chung, MD/PhD wrote:
    > > > >
    > > > > > Kumar wrote:
    > > > >
    > > > > > > > The longer half-life of insulin is due to decreased rates of
    > > > > > > > degradation and not decreased rates of excretion.
    > > > >
    > > > >
    > > > > > > > and so he may need to adjust injected insulin
    > > > >
    > > > >
    > > > > > > Can you explain how decreased rates of degradation of insulin happen?
    > > > >
    > > > >
    > > > > > Loss of nephrons where the degradation occurs.
    > > > >
    > > > >
    > > > >
    > > > > Whether loss of nephrons causes increased or decreased filteration?
    > > >
    > > > Decreased
    > > >
    > > > > On
    > > > > one hand we say lesser filteration on other hand protiens(bigger
    > > > > molecules) start coming into urine on getting DN?
    > > >
    > > > Proteinuria does happen with DN but this does not appreciably alter the
    > > > half-life of insulin.

    > >
    > > I was just comparing the size of molecules with filteration as protiens
    > > are filtered but not insulin on getting DN.??

    >
    > Depends on the protein.


    How? By its size/molecular weight or by its quality?

    > > > > > > What about cluster or crystal formation possibilty of molecules of
    > > > > > > insulin?
    > > > >
    > > > > > There is no reason to invoke this.
    > > > >
    > > > >
    > > > > > > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
    > > > > > > > > stages?
    > > > >
    > > > >
    > > > > > > > Insulin is not excreted in the urine.
    > > > >
    > > > >
    > > > > > > Why when the molecyular weight of insulin is more than 1/4th of
    > > > > > > filteration capacity of kydneys?
    > > > >
    > > > >
    > > > > > You just answered your question by your question.
    > > > >
    > > > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
    > > > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
    > > > > filteration capacity of kidneys (30000 D)?
    > > >
    > > > Insulin is a charged polypeptide that will not get through the
    > > > glomerular basement membrane which is a more effective barrier when a
    > > > macromolecule has a charge.

    > >
    > > Sorry, it is not clear to me.

    >
    > The glomerular basement membrane is **selectively** permeable.


    Good information. Just to clarify more....Whether glomerular
    filteration is by active transport system which don't filter or not
    capable of filtering insulin selectively?

    > > > > > > Moreover capillary permeability for
    > > > > > > insulin is considered as 0.2.
    > > > >
    > > > > > The glomeruli of nephrons of the kidney are considerably less permeable
    > > > > > to polypeptides such as insulin than capillary beds.
    > > > >
    > > > > Can it mean that extra cellular fluids in our tissues will have bigger
    > > > > molecules than as we have in urine alike insulin?
    > > >
    > > > Yes.

    > >
    > > Sorry following question is pending;
    > >> > "Furthermore, adipose

    > > tissue is a major endocrine organ that secretes numerous polypeptide
    > > hormones and cytokines that are proinflammatory and proatherogenic."



    > > Do excess fats in tissues is proinflamatory, proatherogenic,
    > > prodiabetic, proacidosis, procanerous?




    > > > Yes to all the above except for "proacidosis."

    > >
    > > Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?

    >
    > VA ?


    I meant; can greater visceral adiposity or excess fats in tisuues be
    pro-alkaliosis and pro-azoospermia( due to sperm growth arrest at
    spermocytic stage)?

    I want to know relation of greater visceral adiposity or excess fats in
    tisuues with acid, base, water and temperature level.

    >
    > > Whether inflammatory, atherogenic,cancerous, diabetic effects are
    > > pro-acidosis or pro-alkaliosis?

    >
    > The buffering capacity of serum bicarbonate with normal pulmonary
    > function is such that serum pH is well regulated even in the face of
    > most metabolic derangements.


    That is ok, but continious and prolonged regulations in maintaining
    normal pH due to prolonged derangements ( one may be by greater
    visceral adiposity or excess fats in tisuues) may cause progressive or
    degenarative damages. ??
     
  13. 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:
    > > > > > > > Reply against my post no 34 is pending.
    > > > > >
    > > > > > When I sort by date it comes 34 as under;
    > > > > >
    > > > > > 34. Kumar
    > > > > > Jan 22, 11:57 am show options
    > > > > >
    > > > > > Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
    > > > > > From: "Kumar" <[email protected]> - Find messages by this
    > > > > > author
    > > > > > Date: 21 Jan 2006 22:57:57 -0800
    > > > > > Local: Sun, Jan 22 2006 11:57 am
    > > > > > Subject: Re: Fatty Liver
    > > > > > Reply | Reply to Author | Forward | Print | Individual Message | Show
    > > > > > original | Remove | Report Abuse
    > > > > >
    > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > >
    > > > > > > Kumar wrote:
    > > > > >
    > > > > > > > > The longer half-life of insulin is due to decreased rates of
    > > > > > > > > degradation and not decreased rates of excretion.
    > > > > >
    > > > > >
    > > > > > > > > and so he may need to adjust injected insulin
    > > > > >
    > > > > >
    > > > > > > > Can you explain how decreased rates of degradation of insulin happen?
    > > > > >
    > > > > >
    > > > > > > Loss of nephrons where the degradation occurs.
    > > > > >
    > > > > >
    > > > > >
    > > > > > Whether loss of nephrons causes increased or decreased filteration?
    > > > >
    > > > > Decreased
    > > > >
    > > > > > On
    > > > > > one hand we say lesser filteration on other hand protiens(bigger
    > > > > > molecules) start coming into urine on getting DN?
    > > > >
    > > > > Proteinuria does happen with DN but this does not appreciably alter the
    > > > > half-life of insulin.
    > > >
    > > > I was just comparing the size of molecules with filteration as protiens
    > > > are filtered but not insulin on getting DN.??

    > >
    > > Depends on the protein.

    >
    > How? By its size/molecular weight or by its quality?


    All the above.

    > > > > > > > What about cluster or crystal formation possibilty of molecules of
    > > > > > > > insulin?
    > > > > >
    > > > > > > There is no reason to invoke this.
    > > > > >
    > > > > >
    > > > > > > > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
    > > > > > > > > > stages?
    > > > > >
    > > > > >
    > > > > > > > > Insulin is not excreted in the urine.
    > > > > >
    > > > > >
    > > > > > > > Why when the molecyular weight of insulin is more than 1/4th of
    > > > > > > > filteration capacity of kydneys?
    > > > > >
    > > > > >
    > > > > > > You just answered your question by your question.
    > > > > >
    > > > > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
    > > > > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
    > > > > > filteration capacity of kidneys (30000 D)?
    > > > >
    > > > > Insulin is a charged polypeptide that will not get through the
    > > > > glomerular basement membrane which is a more effective barrier when a
    > > > > macromolecule has a charge.
    > > >
    > > > Sorry, it is not clear to me.

    > >
    > > The glomerular basement membrane is **selectively** permeable.

    >
    > Good information. Just to clarify more....Whether glomerular
    > filteration is by active transport system which don't filter or not
    > capable of filtering insulin selectively?


    There is no active transport involved.

    > > > > > > > Moreover capillary permeability for
    > > > > > > > insulin is considered as 0.2.
    > > > > >
    > > > > > > The glomeruli of nephrons of the kidney are considerably less permeable
    > > > > > > to polypeptides such as insulin than capillary beds.
    > > > > >
    > > > > > Can it mean that extra cellular fluids in our tissues will have bigger
    > > > > > molecules than as we have in urine alike insulin?
    > > > >
    > > > > Yes.
    > > >
    > > > Sorry following question is pending;
    > > >> > "Furthermore, adipose
    > > > tissue is a major endocrine organ that secretes numerous polypeptide
    > > > hormones and cytokines that are proinflammatory and proatherogenic."

    >
    >
    > > > Do excess fats in tissues is proinflamatory, proatherogenic,
    > > > prodiabetic, proacidosis, procanerous?

    >
    >
    >
    > > > > Yes to all the above except for "proacidosis."
    > > >
    > > > Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?

    > >
    > > VA ?

    >
    > I meant; can greater visceral adiposity or excess fats in tisuues be
    > pro-alkaliosis and pro-azoospermia( due to sperm growth arrest at
    > spermocytic stage)?


    The latter possibly.

    > I want to know relation of greater visceral adiposity or excess fats in
    > tisuues with acid, base, water and temperature level.


    There should be no significant impact upon homeostatic processes from
    visceral adiposity.

    > > > Whether inflammatory, atherogenic,cancerous, diabetic effects are
    > > > pro-acidosis or pro-alkaliosis?

    > >
    > > The buffering capacity of serum bicarbonate with normal pulmonary
    > > function is such that serum pH is well regulated even in the face of
    > > most metabolic derangements.

    >
    > That is ok, but continious and prolonged regulations in maintaining
    > normal pH due to prolonged derangements ( one may be by greater
    > visceral adiposity or excess fats in tisuues) may cause progressive or
    > degenarative damages. ??


    Unlikely.

    May the LORD help us all to face the great tribulation when the Lamb
    opens the 6th seal possibly in less than a few months (03/29/06), in
    Jesus' most precious and holy name.

    Amen !!!

    Now this is about the works of the four horsemen from the 6th chapter
    of the Book of Revelation (we are now in the 6th year into the third
    millenium after the birth of the Son of Man):

    (1) Crowned rider wielding a bow and riding a white horse:

    "See you on the other side. It's not bad. We are just going to
    sleep." - missive (missile) from one of 12 born-again Christian miners
    who gave up their lives to save the youngest among them after being
    trapped by an explosion in a W.Va mine.

    (2) Rider wielding a sword and riding a fiery red horse:

    Ariel Sharon, the world's hope for lasting peace in the middle east,
    suffers a massive bleeding stroke. Violence and bloodshed in Iraq
    escalates. U.S. now less likely to pull out of Iraq anytime soon.

    (3) Rider wielding a set of food scales and riding a black horse:

    The rate of increase of the number of people worldwide using the
    2PD-OMER Approach (which advocates the use of food scales) accelerates
    with growing worldwide concerns about the obesity epidemic:

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

    Meanwhile, folks like Bob Pastorio who refuse to use this Approach are
    heard muttering that an omer is not a weight measure but a volume
    measure somewhere between one and three quarts depending on what the
    food is and that liquid foods like milk (emulsified oil) and wine
    should not be counted toward daily intake.

    (4) Rider on a pale horse given the authority to kill a fourth of the
    world's population "by sword, famine and plague, and by the wild beasts
    of the earth":

    The H5N1 Avian Flu Pandemic seems to be starting in Turkey:

    http://tinyurl.com/amj4a

    Yes, the migratory birds spreading H5N1 virus are wild beasts of the
    earth.

    The 5th seal has been opened and glimpses of "the souls of those who
    had been slain because of the Word of GOD and the testimony they had
    maintained" (Revelation 6:9) can be seen in the newly released
    documentary "End of the Spear."

    When will the sun "turn black like sackcloth made of goat hair"
    (Revelation 6:12b) ?

    It will turn black during the total solar eclipse that will happen
    **also** in Turkey on Wednesday 03/29/2006 at around 14:00 hrs LT.

    http://tinyurl.com/dcj7w

    The order of darkening of the following ancient cities in Turkey:

    (1) Ephesus
    (2) Smyrna
    (3) Pergamum
    (4) Thyatira
    (5) Sardis
    (6) Philadelphia
    (7) Laodicea

    Will be the same order that Christ Jesus used to address the seven
    churches:

    "Write on a scroll what you see and send it to the seven churches: to
    Ephesus, Smyrna, Pergamum, Thyratira, Sardis, Philadelphia and
    Laodicea." (Revelation 1:11)

    Would be more than happy 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 (01/26/06) 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/cbn2r
     
  14. Enrico C

    Enrico C Guest

    On 22 Jan 2006 21:15:46 -0800, Kumar wrote in
    <news:[email protected]> on
    alt.support.diabetes,sci.med.cardiology,sci.med,sci.med.nutrition :

    >>> Reply against my post no 34 is pending.

    >
    > When I sort by date it comes 34 as under;
    >
    > 34. Kumar


    You can use a full Google link, or a Message-Id, to univocally
    identify a post...



    X'Posted to: alt.support.diabetes,sci.med.nutrition

    --
    Enrico C

    * cut the ending "cut-togli.invalid" string when replying by email *
     
  15. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    >> > > >
    > > > > > > > The longer half-life of insulin is due to decreased rates of
    > > > > > > > degradation and not decreased rates of excretion.
    > > > >
    > > > >
    > > > > > > > and so he may need to adjust injected insulin
    > > > >
    > > > >
    > > > > > > Can you explain how decreased rates of degradation of insulin happen?
    > > > >
    > > > >
    > > > > > Loss of nephrons where the degradation occurs.
    > > > >
    > > > >
    > > > >
    > > > > Whether loss of nephrons causes increased or decreased filteration?
    > > >
    > > > Decreased
    > > >
    > > > > On
    > > > > one hand we say lesser filteration on other hand protiens(bigger
    > > > > molecules) start coming into urine on getting DN?
    > > >
    > > > Proteinuria does happen with DN but this does not appreciably alter the
    > > > half-life of insulin.

    > >
    > > I was just comparing the size of molecules with filteration as protiens
    > > are filtered but not insulin on getting DN.??

    >
    > Depends on the protein.
    > > > > > > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
    > > > > > > > > stages?
    > > > >
    > > > >
    > > > > > > > Insulin is not excreted in the urine.
    > > > >
    > > > >
    > > > > > > Why when the molecyular weight of insulin is more than 1/4th of
    > > > > > > filteration capacity of kydneys?
    > > > >
    > > > >
    > > > > > You just answered your question by your question.
    > > > >
    > > > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
    > > > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
    > > > > filteration capacity of kidneys (30000 D)?
    > > >
    > > > Insulin is a charged polypeptide that will not get through the
    > > > glomerular basement membrane which is a more effective barrier when a
    > > > macromolecule has a charge.

    > >
    > > Sorry, it is not clear to me.

    >
    > The glomerular basement membrane is **selectively** permeable.


    '...As kidney failure progresses, less insulin is excreted, so smaller
    doses may be needed to control glucose levels.
    Complications
    Possible complications include:hypoglycemia (from decreased excretion
    of insulin)
    http://www.nlm.nih.gov/medlineplus/ency/article/000494.htm '

    The above medlineplus quote indicate that insulin is excreted. Can you
    check tell about it again?
     
  16. Kumar

    Kumar Guest


    > > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > >
    > > > > > > > Kumar wrote:
    > > > > > >
    > > > > > > > > > The longer half-life of insulin is due to decreased rates of
    > > > > > > > > > degradation and not decreased rates of excretion.
    > > > > > >
    > > > > > >
    > > > > > > > > > and so he may need to adjust injected insulin
    > > > > > >
    > > > > > >
    > > > > > > > > Can you explain how decreased rates of degradation of insulin happen?
    > > > > > >
    > > > > > >
    > > > > > > > Loss of nephrons where the degradation occurs.
    > > > > > >
    > > > > > >
    > > > > > >
    > > > > > > Whether loss of nephrons causes increased or decreased filteration?
    > > > > >
    > > > > > Decreased
    > > > > >
    > > > > > > On
    > > > > > > one hand we say lesser filteration on other hand protiens(bigger
    > > > > > > molecules) start coming into urine on getting DN?
    > > > > >
    > > > > > Proteinuria does happen with DN but this does not appreciably alter the
    > > > > > half-life of insulin.
    > > > >
    > > > > I was just comparing the size of molecules with filteration as protiens
    > > > > are filtered but not insulin on getting DN.??
    > > >
    > > > Depends on the protein.

    > >
    > > How? By its size/molecular weight or by its quality?

    >
    > All the above.


    How by its quality?

    > > > > > > > > > Insulin is not excreted in the urine.


    My previous post pls.

    > > > > > >
    > > > > > >
    > > > > > > > > Why when the molecyular weight of insulin is more than 1/4th of
    > > > > > > > > filteration capacity of kydneys?
    > > > > > >
    > > > > > >
    > > > > > > > You just answered your question by your question.
    > > > > > >
    > > > > > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
    > > > > > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
    > > > > > > filteration capacity of kidneys (30000 D)?
    > > > > >
    > > > > > Insulin is a charged polypeptide that will not get through the
    > > > > > glomerular basement membrane which is a more effective barrier when a
    > > > > > macromolecule has a charge.
    > > > >
    > > > > Sorry, it is not clear to me.
    > > >
    > > > The glomerular basement membrane is **selectively** permeable.

    > >
    > > Good information. Just to clarify more....Whether glomerular
    > > filteration is by active transport system which don't filter or not
    > > capable of filtering insulin selectively?

    >
    > There is no active transport involved.
    >
    > > > > > > > > Moreover capillary permeability for
    > > > > > > > > insulin is considered as 0.2.
    > > > > > >
    > > > > > > > The glomeruli of nephrons of the kidney are considerably less permeable
    > > > > > > > to polypeptides such as insulin than capillary beds.
    > > > > > >
    > > > > > > Can it mean that extra cellular fluids in our tissues will have bigger
    > > > > > > molecules than as we have in urine alike insulin?
    > > > > >
    > > > > > Yes.
    > > > >
    > > > > Sorry following question is pending;
    > > > >> > "Furthermore, adipose
    > > > > tissue is a major endocrine organ that secretes numerous polypeptide
    > > > > hormones and cytokines that are proinflammatory and proatherogenic."

    > >
    > >
    > > > > Do excess fats in tissues is proinflamatory, proatherogenic,
    > > > > prodiabetic, proacidosis, procanerous?

    > >
    > >
    > >
    > > > > > Yes to all the above except for "proacidosis."
    > > > >
    > > > > Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?
    > > >
    > > > VA ?

    > >
    > > I meant; can greater visceral adiposity or excess fats in tisuues be
    > > pro-alkaliosis and pro-azoospermia( due to sperm growth arrest at
    > > spermocytic stage)?

    >
    > The latter possibly.
    >
    > > I want to know relation of greater visceral adiposity or excess fats in
    > > tisuues with acid, base, water and temperature level.

    >
    > There should be no significant impact upon homeostatic processes from
    > visceral adiposity.


    What about from excess subcutaneous fats depositions? Does it effect
    acid/base balance? Pls don't consider what body can correct for this
    purpose.

    > > > > Whether inflammatory, atherogenic,cancerous, diabetic effects are
    > > > > pro-acidosis or pro-alkaliosis?
    > > >
    > > > The buffering capacity of serum bicarbonate with normal pulmonary
    > > > function is such that serum pH is well regulated even in the face of
    > > > most metabolic derangements.

    > >
    > > That is ok, but continious and prolonged regulations in maintaining
    > > normal pH due to prolonged derangements ( one may be by greater
    > > visceral adiposity or excess fats in tisuues) may cause progressive or
    > > degenarative damages. ??

    >
    > Unlikely.


    Do you mean that continious and prolonged hammering to body system for
    the control of acid/base derangements can have no acute, chronic or
    progressive damages?
     
  17. Kumar wrote:
    > > > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > >
    > > > > > > > > Kumar wrote:
    > > > > > > >
    > > > > > > > > > > The longer half-life of insulin is due to decreased rates of
    > > > > > > > > > > degradation and not decreased rates of excretion.
    > > > > > > >
    > > > > > > >
    > > > > > > > > > > and so he may need to adjust injected insulin
    > > > > > > >
    > > > > > > >
    > > > > > > > > > Can you explain how decreased rates of degradation of insulin happen?
    > > > > > > >
    > > > > > > >
    > > > > > > > > Loss of nephrons where the degradation occurs.
    > > > > > > >
    > > > > > > >
    > > > > > > >
    > > > > > > > Whether loss of nephrons causes increased or decreased filteration?
    > > > > > >
    > > > > > > Decreased
    > > > > > >
    > > > > > > > On
    > > > > > > > one hand we say lesser filteration on other hand protiens(bigger
    > > > > > > > molecules) start coming into urine on getting DN?
    > > > > > >
    > > > > > > Proteinuria does happen with DN but this does not appreciably alter the
    > > > > > > half-life of insulin.
    > > > > >
    > > > > > I was just comparing the size of molecules with filteration as protiens
    > > > > > are filtered but not insulin on getting DN.??
    > > > >
    > > > > Depends on the protein.
    > > >
    > > > How? By its size/molecular weight or by its quality?

    > >
    > > All the above.

    >
    > How by its quality?


    By charge.

    > > > > > > > > > > Insulin is not excreted in the urine.

    >
    > My previous post pls.


    Already asked and answered.

    > > > > > > >
    > > > > > > >
    > > > > > > > > > Why when the molecyular weight of insulin is more than 1/4th of
    > > > > > > > > > filteration capacity of kydneys?
    > > > > > > >
    > > > > > > >
    > > > > > > > > You just answered your question by your question.
    > > > > > > >
    > > > > > > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
    > > > > > > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
    > > > > > > > filteration capacity of kidneys (30000 D)?
    > > > > > >
    > > > > > > Insulin is a charged polypeptide that will not get through the
    > > > > > > glomerular basement membrane which is a more effective barrier when a
    > > > > > > macromolecule has a charge.
    > > > > >
    > > > > > Sorry, it is not clear to me.
    > > > >
    > > > > The glomerular basement membrane is **selectively** permeable.
    > > >
    > > > Good information. Just to clarify more....Whether glomerular
    > > > filteration is by active transport system which don't filter or not
    > > > capable of filtering insulin selectively?

    > >
    > > There is no active transport involved.
    > >
    > > > > > > > > > Moreover capillary permeability for
    > > > > > > > > > insulin is considered as 0.2.
    > > > > > > >
    > > > > > > > > The glomeruli of nephrons of the kidney are considerably less permeable
    > > > > > > > > to polypeptides such as insulin than capillary beds.
    > > > > > > >
    > > > > > > > Can it mean that extra cellular fluids in our tissues will have bigger
    > > > > > > > molecules than as we have in urine alike insulin?
    > > > > > >
    > > > > > > Yes.
    > > > > >
    > > > > > Sorry following question is pending;
    > > > > >> > "Furthermore, adipose
    > > > > > tissue is a major endocrine organ that secretes numerous polypeptide
    > > > > > hormones and cytokines that are proinflammatory and proatherogenic."
    > > >
    > > >
    > > > > > Do excess fats in tissues is proinflamatory, proatherogenic,
    > > > > > prodiabetic, proacidosis, procanerous?
    > > >
    > > >
    > > >
    > > > > > > Yes to all the above except for "proacidosis."
    > > > > >
    > > > > > Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?
    > > > >
    > > > > VA ?
    > > >
    > > > I meant; can greater visceral adiposity or excess fats in tisuues be
    > > > pro-alkaliosis and pro-azoospermia( due to sperm growth arrest at
    > > > spermocytic stage)?

    > >
    > > The latter possibly.
    > >
    > > > I want to know relation of greater visceral adiposity or excess fats in
    > > > tisuues with acid, base, water and temperature level.

    > >
    > > There should be no significant impact upon homeostatic processes from
    > > visceral adiposity.

    >
    > What about from excess subcutaneous fats depositions? Does it effect
    > acid/base balance? Pls don't consider what body can correct for this
    > purpose.


    Subcutaneous fat is largely avascular.

    > > > > > Whether inflammatory, atherogenic,cancerous, diabetic effects are
    > > > > > pro-acidosis or pro-alkaliosis?
    > > > >
    > > > > The buffering capacity of serum bicarbonate with normal pulmonary
    > > > > function is such that serum pH is well regulated even in the face of
    > > > > most metabolic derangements.
    > > >
    > > > That is ok, but continious and prolonged regulations in maintaining
    > > > normal pH due to prolonged derangements ( one may be by greater
    > > > visceral adiposity or excess fats in tisuues) may cause progressive or
    > > > degenarative damages. ??

    > >
    > > Unlikely.

    >
    > Do you mean that continious and prolonged hammering to body system for
    > the control of acid/base derangements can have no acute, chronic or
    > progressive damages?


    Our bodies are wonderfully made by the LORD :))

    Would be more than happy 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 (01/26/06):

    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/cbn2r
     
  18. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > > > > > > > Andrew B. Chung, MD/PhD wrote:
    > > > > > > > >
    > > > > > > > > > Kumar wrote:
    > > > > > > > >
    > > > > > > > > > > > The longer half-life of insulin is due to decreased rates of
    > > > > > > > > > > > degradation and not decreased rates of excretion.
    > > > > > > > >
    > > > > > > > >
    > > > > > > > > > > > and so he may need to adjust injected insulin
    > > > > > > > >
    > > > > > > > >
    > > > > > > > > > > Can you explain how decreased rates of degradation of insulin happen?
    > > > > > > > >
    > > > > > > > >
    > > > > > > > > > Loss of nephrons where the degradation occurs.
    > > > > > > > >
    > > > > > > > >
    > > > > > > > >
    > > > > > > > > Whether loss of nephrons causes increased or decreased filteration?
    > > > > > > >
    > > > > > > > Decreased
    > > > > > > >
    > > > > > > > > On
    > > > > > > > > one hand we say lesser filteration on other hand protiens(bigger
    > > > > > > > > molecules) start coming into urine on getting DN?
    > > > > > > >
    > > > > > > > Proteinuria does happen with DN but this does not appreciably alter the
    > > > > > > > half-life of insulin.
    > > > > > >
    > > > > > > I was just comparing the size of molecules with filteration as protiens
    > > > > > > are filtered but not insulin on getting DN.??
    > > > > >
    > > > > > Depends on the protein.
    > > > >
    > > > > How? By its size/molecular weight or by its quality?
    > > >
    > > > All the above.

    > >
    > > How by its quality?

    >
    > By charge.


    This looks to be a special aspect. Can you tell some more details, what
    is this charge and how it can effect insulin excretion?
    > > > > > > > > > > > Insulin is not excreted in the urine.

    > >
    > > My previous post pls.

    >
    > Already asked and answered.

    My previous post was:-

    "...As kidney failure progresses, less insulin is excreted, so smaller
    doses may be needed to control glucose levels.
    Complications
    Possible complications include:hypoglycemia (from decreased excretion
    of insulin)
    http://www.nlm.nih.gov/medlineplus/ency/article/000494.htm "

    The above medlineplus quote indicate that insulin is excreted. Can you
    check tell about it again?



    >
    > > > > > > > >
    > > > > > > > >
    > > > > > > > > > > Why when the molecyular weight of insulin is more than 1/4th of
    > > > > > > > > > > filteration capacity of kydneys?
    > > > > > > > >
    > > > > > > > >
    > > > > > > > > > You just answered your question by your question.
    > > > > > > > >
    > > > > > > > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
    > > > > > > > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
    > > > > > > > > filteration capacity of kidneys (30000 D)?
    > > > > > > >
    > > > > > > > Insulin is a charged polypeptide that will not get through the
    > > > > > > > glomerular basement membrane which is a more effective barrier when a
    > > > > > > > macromolecule has a charge.
    > > > > > >
    > > > > > > Sorry, it is not clear to me.
    > > > > >
    > > > > > The glomerular basement membrane is **selectively** permeable.
    > > > >
    > > > > Good information. Just to clarify more....Whether glomerular
    > > > > filteration is by active transport system which don't filter or not
    > > > > capable of filtering insulin selectively?
    > > >
    > > > There is no active transport involved.
    > > >
    > > > > > > > > > > Moreover capillary permeability for
    > > > > > > > > > > insulin is considered as 0.2.
    > > > > > > > >
    > > > > > > > > > The glomeruli of nephrons of the kidney are considerably less permeable
    > > > > > > > > > to polypeptides such as insulin than capillary beds.
    > > > > > > > >
    > > > > > > > > Can it mean that extra cellular fluids in our tissues will have bigger
    > > > > > > > > molecules than as we have in urine alike insulin?
    > > > > > > >
    > > > > > > > Yes.
    > > > > > >
    > > > > > > Sorry following question is pending;
    > > > > > >> > "Furthermore, adipose
    > > > > > > tissue is a major endocrine organ that secretes numerous polypeptide
    > > > > > > hormones and cytokines that are proinflammatory and proatherogenic."
    > > > >
    > > > >
    > > > > > > Do excess fats in tissues is proinflamatory, proatherogenic,
    > > > > > > prodiabetic, proacidosis, procanerous?
    > > > >
    > > > >
    > > > >
    > > > > > > > Yes to all the above except for "proacidosis."
    > > > > > >
    > > > > > > Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?
    > > > > >
    > > > > > VA ?
    > > > >
    > > > > I meant; can greater visceral adiposity or excess fats in tisuues be
    > > > > pro-alkaliosis and pro-azoospermia( due to sperm growth arrest at
    > > > > spermocytic stage)?
    > > >
    > > > The latter possibly.
    > > >
    > > > > I want to know relation of greater visceral adiposity or excess fats in
    > > > > tisuues with acid, base, water and temperature level.
    > > >
    > > > There should be no significant impact upon homeostatic processes from
    > > > visceral adiposity.

    > >
    > > What about from excess subcutaneous fats depositions? Does it effect
    > > acid/base balance? Pls don't consider what body can correct for this
    > > purpose.

    >
    > Subcutaneous fat is largely avascular.


    Visceral?? Are these vascular? If yes can they effect acid/base and
    temperature balance?

    > > > > > > Whether inflammatory, atherogenic,cancerous, diabetic effects are
    > > > > > > pro-acidosis or pro-alkaliosis?
    > > > > >
    > > > > > The buffering capacity of serum bicarbonate with normal pulmonary
    > > > > > function is such that serum pH is well regulated even in the face of
    > > > > > most metabolic derangements.
    > > > >
    > > > > That is ok, but continious and prolonged regulations in maintaining
    > > > > normal pH due to prolonged derangements ( one may be by greater
    > > > > visceral adiposity or excess fats in tisuues) may cause progressive or
    > > > > degenarative damages. ??
    > > >
    > > > Unlikely.

    > >
    > > Do you mean that continious and prolonged hammering to body system for
    > > the control of acid/base derangements can have no acute, chronic or
    > > progressive damages?

    >
    > Our bodies are wonderfully made by the LORD :))


    Yes, but can't there be some limitations as it is made by lord but is
    not a Lord?

    Anyway, can bicarbonate imbalance in blood and three compartments be
    related to persistent and uncontrolled elevated blood glucose levels in
    blood. In other sense, can diabetics with somewhat acidosis find
    difficulty in controling their elevated blood glucose than diabetics
    with somewhat acidosis? Insulin role in Potassium shifting
    intracellularily and potassium relation with acidosis and osmolity may
    be considered for such bicarboate effect. Why sodium bicarbonate is
    considered as systematic antacid others not?

    I am also interested much to understand diferenciating effects by
    acid-blockers and antacids on internal environment in view of that
    gastric acid secretion may cause "alkaline tide" temporarily internally
    as its production relese bicarbonate inside blood. Opposite is related
    to acidic effect inside on pacreatic bicarbonate secretion.
     
  19. Kumar

    Kumar Guest

    Andrew B. Chung, MD/PhD wrote:
    > Kumar wrote:
    > > In continuance to my last post......
    > >
    > > "Insulin
    > >
    > > Monomers, Dimers and Hexamers
    > > http://www.med.unibs.it/~marchesi/pps97/course/section11/insulin.html
    > >
    > > The above link suggests different possible forms and variants of
    > > insulin. Insulin as monomer is only active and its polymers are
    > > ineffective. As such any persistance of insulin in polymer may also be
    > > a reason to getting insulin resistance or insenstivity to insulin. As
    > > such insulin in polymer form may not be filtered whereas it can be
    > > filtered or filtered lesser in monomer and dimer form....may also be a
    > > reason to getting hyperglycemia. Furthur pH and insulin concentration
    > > seems to be two reasons responsible for its polymerization. We may then
    > > have to think about alterations in pH, Zinc levels, excess insulin
    > > concentration--naturally, medicated or injected to understand
    > > senstivity and non-senstivity of insulin.
    > >
    > > Can you comment on it?

    >
    > Insulin is not the only polypeptide that is denatured in
    > non-physiological conditions.


    Reply against my previous post # 54 pending pls.

    Yes but I am thinking about insulin. Can a person become diabetic type2
    due to persistance of his insulin molecules in aggregated or polymer
    state? How such conditions(polymerization of insulin molecules) be
    improved by some food changes or by medicines?

    At some links it is indicated that urea, acetic acid..can cause
    monomerization of insulin. Can vinegar do something for this? Can
    excess BUN be related to better utilization of insulin in monomeric
    form--so needed to lower insulin injections????
     
  20. Kumar wrote:
    >
    > Andrew B. Chung, MD/PhD wrote:
    > > Kumar wrote:
    > > > In continuance to my last post......
    > > >
    > > > "Insulin
    > > >
    > > > Monomers, Dimers and Hexamers
    > > > http://www.med.unibs.it/~marchesi/pps97/course/section11/insulin.html
    > > >
    > > > The above link suggests different possible forms and variants of
    > > > insulin. Insulin as monomer is only active and its polymers are
    > > > ineffective. As such any persistance of insulin in polymer may also be
    > > > a reason to getting insulin resistance or insenstivity to insulin. As
    > > > such insulin in polymer form may not be filtered whereas it can be
    > > > filtered or filtered lesser in monomer and dimer form....may also be a
    > > > reason to getting hyperglycemia. Furthur pH and insulin concentration
    > > > seems to be two reasons responsible for its polymerization. We may then
    > > > have to think about alterations in pH, Zinc levels, excess insulin
    > > > concentration--naturally, medicated or injected to understand
    > > > senstivity and non-senstivity of insulin.
    > > >
    > > > Can you comment on it?

    > >
    > > Insulin is not the only polypeptide that is denatured in
    > > non-physiological conditions.

    >
    > Reply against my previous post # 54 pending pls.
    >
    > Yes but I am thinking about insulin. Can a person become diabetic type2
    > due to persistance of his insulin molecules in aggregated or polymer
    > state?


    No. This person would die from the non-physiological conditions first.

    Would be more than happy 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 (01/19/2006)
    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/b6xwk
     
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