Re: Fatty Liver

  • Thread starter Andrew B. Chung, MD/PhD
  • Start date



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

How? There can be slow or lesser utilization due to any condition on
some monomerization of some polymerized insulin alike injected long
acting insulin which is in polymerized state.

Have you read my post #55(not 54)?
 
Kumar wrote:
> Andrew B. Chung, MD/PhD wrote:
> > 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.

> How?


The conduction system of the heart is very sensitive to perturbations
in homeostasis. These pertubations have the potential for triggering
lethal dysrhythmias.

> There can be slow or lesser utilization due to any condition on
> some monomerization of some polymerized insulin alike injected long
> acting insulin which is in polymerized state.


The latter is non-physiological.

> Have you read my post #55(not 54)?


Don't know which post you are referring to.

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

> > How?

>
> The conduction system of the heart is very sensitive to perturbations
> in homeostasis. These pertubations have the potential for triggering
> lethal dysrhythmias.


How insulin polymerization and monomerization is related to it?

Sorry, other relavent question:-

Can excess or low levels and effects of insulin cause excess or low
contractions in muscles esp. in low back muscles resulting into low
back pain?


> > There can be slow or lesser utilization due to any condition on
> > some monomerization of some polymerized insulin alike injected long
> > acting insulin which is in polymerized state.

>
> The latter is non-physiological.
>
> > Have you read my post #55(not 54)?

>
> Don't know which post you are referring to.


It was #55 if sorted by date. Any way I am pasting below again:-

55. Kumar
Jan 24, 8:41 am show options



Andrew B. Chung, MD/PhD wrote:




- Hide quoted text -
- Show quoted text -

> 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?




- Hide quoted text -
- Show quoted text -

> > > > > > > > > > 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?



- Hide quoted text -
- Show quoted text -

> > > > > > 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
 
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:
> > > > > 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.
> > > How?

> >
> > The conduction system of the heart is very sensitive to perturbations
> > in homeostasis. These pertubations have the potential for triggering
> > lethal dysrhythmias.

>
> How insulin polymerization and monomerization is related to it?


Unrelated.

> Sorry, other relavent question:-
>
> Can excess or low levels and effects of insulin cause excess or low
> contractions in muscles esp. in low back muscles resulting into low
> back pain?


There is no known association. Would suggest you inform your doctor
about the symptoms you are having.

> > > There can be slow or lesser utilization due to any condition on
> > > some monomerization of some polymerized insulin alike injected long
> > > acting insulin which is in polymerized state.

> >
> > The latter is non-physiological.
> >
> > > Have you read my post #55(not 54)?

> >
> > Don't know which post you are referring to.

>
> It was #55 if sorted by date. Any way I am pasting below again:-
>
> 55. Kumar
> Jan 24, 8:41 am show options
>
>
>
> Andrew B. Chung, MD/PhD wrote:
>
>
>
>
> - Hide quoted text -
> - Show quoted text -
>
> > 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 by the kidneys (i.e. it is not present in
urine).

> > > > > > > > > > > > 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?


The medlineplus article is wrong about insulin excretion. Insulin is a
polypeptide that is inactivated not by excretion but by catabolism.
The following article addresses this point in the setting of DKA which
is a severe perturbation of homeostatic mechanisms that maintain
physiological conditions:

http://tinyurl.com/b2xlp

>
>
> - Hide quoted text -
> - Show quoted text -
>
> > > > > > > > > > > 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?


They are more vascular.

> If yes can they effect acid/base and
> temperature balance?


No.


>
> - Hide quoted text -
> - Show quoted text -
>
> > > > > > > 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?


There are no limitations for those who place their hope and faith in
the 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?


Because of the presence of carbonic anhydrase in the blood combined
with the efficiency of the lungs for gas exchange.

>
> 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


Will be available to 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/b6xwk
 
Andrew B. Chung, MD/PhD 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:
> > > > > > 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.
> > > > How?
> > >
> > > The conduction system of the heart is very sensitive to perturbations
> > > in homeostasis. These pertubations have the potential for triggering
> > > lethal dysrhythmias.

> >
> > How insulin polymerization and monomerization is related to it?

>
> Unrelated.
>
> > Sorry, other relavent question:-
> >
> > Can excess or low levels and effects of insulin cause excess or low
> > contractions in muscles esp. in low back muscles resulting into low
> > back pain?

>
> There is no known association. Would suggest you inform your doctor
> about the symptoms you are having.


Thanks it is resolved.

> > > > There can be slow or lesser utilization due to any condition on
> > > > some monomerization of some polymerized insulin alike injected long
> > > > acting insulin which is in polymerized state.
> > >
> > > The latter is non-physiological.
> > >
> > > > Have you read my post #55(not 54)?
> > >
> > > Don't know which post you are referring to.

> >
> > It was #55 if sorted by date. Any way I am pasting below again:-
> >
> > 55. Kumar
> > Jan 24, 8:41 am show options
> >
> >
> >
> > Andrew B. Chung, MD/PhD wrote:
> >
> >
> >
> >
> > - Hide quoted text -
> > - Show quoted text -
> >
> > > 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 by the kidneys (i.e. it is not present in
> urine).



>
> > > > > > > > > > > > > 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?

>
> The medlineplus article is wrong about insulin excretion. Insulin is a
> polypeptide that is inactivated not by excretion but by catabolism.
> The following article addresses this point in the setting of DKA which
> is a severe perturbation of homeostatic mechanisms that maintain
> physiological conditions:
>
> http://tinyurl.com/b2xlp


"Insulin requirements are often altered, either being increased due to
insulin resistance or decreased due to impairment clearance of
circulatory insulin(4).
"In uremic patients (both diabetic and no diabetic) insulin secretion
by b cells of the pancreas is reduced and the responsiveness of
peripheral tissues (e.g muscles) to insulin is depressed. On the other
hand the rate of insulin catabolism (renal and extra renal) is
decreased and therefore the half life of any insulin present in the
circulation is prolonged. Thus insulin should be given in smaller than
usual doses."

Thanks for good link.

How insulin secretion by b cells of the pancreas is reduced and the
responsiveness of peripheral tissues (e.g muscles) to insulin is
depressed in uremic patients?

What does it mean:rate of insulin catabolism (renal and extra renal) is
decreased? Whether renal catabolism is not excretion/ renal loss of
insulin? I have one thought; Can it be possible that insulin is
degraded or denatured due to more acidic or alkaline environment as
present during filtretion via kidneys so insulin in its origional form
is not traced in urine?


>>

>
> >
> > - Hide quoted text -
> > - Show quoted text -
> >
> > > > > > > > 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?

>
> There are no limitations for those who place their hope and faith in
> the 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?

>
> Because of the presence of carbonic anhydrase in the blood combined
> with the efficiency of the lungs for gas exchange.
>
> >
> > 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

>
> Will be available to 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/b6xwk