Re: Insulin related?

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



Kumar wrote:
> Andrew B. Chung, MD/PhD wrote:
> > Kumar wrote:
> > > Andrew B. Chung, MD/PhD wrote:
> > > > Kumar wrote:
> > > >
> > > > There can be clinically significant lactic acidosis without elevation
> > > > in LDH isoenzymes.
> > > >
> > > "" LDH is most often measured to evaluate the presence of tissue
> > > damage. The enzyme LDH is in many body tissues, especially the heart,
> > > liver, kidney, skeletal muscle, brain, blood cells, and lungs.
> > >
> > > LDH catalyzes the interconversion of pyruvate and lactate. Exercising
> > > muscles convert (and red blood cells metabolize) glucose to lactate.
> > > Lactate is released into the blood and is eventually taken up by the
> > > liver. The liver converts lactate back to glucose and releases glucose
> > > into the blood. This glucose is then taken up by resting muscles, red
> > > blood cells, and other
> > > tissues.http://www.nlm.nih.gov/medlineplus/ency/article/003471.htm ""
> > >
> > > Can't elevated lactic acid damage tissue?
> >
> > Not under physiological conditions.
> >
> Can elevated lactic acid at any part cause pain in that part?

Not under physiological conditions.

> > > Can't tissue before damage be
> > > treated alike Exercising/exerting muscles resulting into lactate
> > > accumulation and some acidosis effect?
> >
> > Yes.
> >
>
> > >
> > > > > > > Can't elevated LDH be an indicator that higher lactate/lactic acid is
> > > > > > > there for conversion into pyruvate?
> > > > > >
> > > > > > Not under physiological conditions.
> > > > > How these raise serum pH--by absorption of antacids or by opposte
> > > > > effect due to more secretion of HCl to neutralize antacids in stomach
> > > > > or by alkaline tide as I indicated?
> > > >
> > > > Alkaline substances raise pH. That is their nature because they bind
> > > > up H+ protons reducing their concentration.
> > > >
> > > Yes but how antacids effects internally in blood?
> >
> > It reacts to reduce the concentration of H+ protons.
> >
> On absorption or otherwise?

Chemical reaction with a base.

> > > > > > > Furthur, can it be possible that insulin esp.long term, if injected in
> > > > > > > fat tissues don't reach to blood?
> > > > > >
> > > > > > No.
> > > > > >
> > > > > > > If yes, what can resist it except
> > > > > > > distance? Can there be some defects by excess fats or some fatty
> > > > > > > degeneration and scarring alike in liver Cirrhosis which may interfere
> > > > > > > in insulin transport?
> > > > > >
> > > > > > No.
> > > > > >
> > > > > What does it mean that it can become non-physyological in fats?
> > > >
> > > > It does not mean anything. Fats are physiological.
> > > >
> > > You told insulin can be non-physiological in fats. What does it mean?
> >
> > Local environments within adipose tissue compartments can be rendered
> > nonphysiological for extended periods of time without affecting
> > homeostasis of the vascular compartment.
> >
> By local environment you mean normal or altered?

Either.

> Will then insulin be degraded ?

No.

> Will such insulin can cause some
> irritation or any other disorder?

No.

> Is it alike fatty lever and fatty degenarations?

No.

> Can fatty degerations
> are possible other than in liver and heart?

You probably mean fatty infiltration.

> If yes, which are other
> parts?

Pancreas and spleen can also have fatty infiltration.

LORD willing, will be available to "glow" and chat about this and other
things like cardiology, diabetes, cooking and nutrition that interest
those following this thread here during the next on-line chat now
(02/09/06):

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/8juld
 
Andrew B. Chung, MD/PhD wrote:
> Kumar wrote:
> > > > Can't elevated lactic acid damage tissue?
> > >
> > > Not under physiological conditions.
> > >
> > Can elevated lactic acid at any part cause pain in that part?
>
> Not under physiological conditions.
>
How anyone get pain on any inflammation?

> > > > Can't tissue before damage be
> > > > treated alike Exercising/exerting muscles resulting into lactate
> > > > accumulation and some acidosis effect?
> > >
> > > Yes.
> > > > > > > Not under physiological conditions.
> > > > > > How these raise serum pH--by absorption of antacids or by opposte
> > > > > > effect due to more secretion of HCl to neutralize antacids in stomach
> > > > > > or by alkaline tide as I indicated?
> > > > >
> > > > > Alkaline substances raise pH. That is their nature because they bind
> > > > > up H+ protons reducing their concentration.
> > > > >
> > > > Yes but how antacids effects internally in blood?
> > >
> > > It reacts to reduce the concentration of H+ protons.
> > >
> > On absorption or otherwise?
>
> Chemical reaction with a base.
>
On excessive intake of antacids, whether these are absorbed in blood or
not? If no, how these can act as base and raise blood and urine pH?

> > > > > > > > Furthur, can it be possible that insulin esp.long term, if injected in
> > > > > > > > fat tissues don't reach to blood?
> > > > > > >
> > > > > > > No.
> > > > > > >
> > > > > > > > If yes, what can resist it except
> > > > > > > > distance? Can there be some defects by excess fats or some fatty
> > > > > > > > degeneration and scarring alike in liver Cirrhosis which may interfere
> > > > > > > > in insulin transport?
> > > > > > >
> > > > > > > No.
> > > > > > >
> > > > > > What does it mean that it can become non-physyological in fats?
> > > > >
> > > > > It does not mean anything. Fats are physiological.
> > > > >
> > > > You told insulin can be non-physiological in fats. What does it mean?
> > >
> > > Local environments within adipose tissue compartments can be rendered
> > > nonphysiological for extended periods of time without affecting
> > > homeostasis of the vascular compartment.
> > >
> > By local environment you mean normal or altered?
>
> Either.
>
Do You mean Local environments within adipose tissue compartments can
be rendered
nonphysiological for extended periods of time in general or will ir be
nonphysiological just for insulin?
> > Will then insulin be degraded ?
>
> No.
>
Will then injected insulin as such in fats, be stored for extended
periods of time? If yes, can it be release excessively sometimes in
blood?

> > Can fatty degerations
> > are possible other than in liver and heart?
>
> You probably mean fatty infiltration.
>
Yes and damages done by such fatty infilterations. I think it is now
called as fatty changes. Whether any imbalance in K or in sulphur
containing protien cause fatty infiltrations and fatty degenarations?
One, Potassium sulphate based healing agent in one alt. system is
indicated for fatty degenarations. It is also indicated for uremia. Can
there be some link between it with fatty infiltrations and elevated
BUN?
> > If yes, which are other
> > parts?
>
> Pancreas and spleen can also have fatty infiltration.
>
Muscles and testis?
 
Kumar wrote:
> Andrew B. Chung, MD/PhD wrote:
> > Kumar wrote:
> > > > > Can't elevated lactic acid damage tissue?
> > > >
> > > > Not under physiological conditions.
> > > >
> > > Can elevated lactic acid at any part cause pain in that part?
> >
> > Not under physiological conditions.
> >
> How anyone get pain on any inflammation?

Through the stimulation of the nerve endings of pain fibers.

> > > > > Can't tissue before damage be
> > > > > treated alike Exercising/exerting muscles resulting into lactate
> > > > > accumulation and some acidosis effect?
> > > >
> > > > Yes.
> > > > > > > > Not under physiological conditions.
> > > > > > > How these raise serum pH--by absorption of antacids or by opposte
> > > > > > > effect due to more secretion of HCl to neutralize antacids in stomach
> > > > > > > or by alkaline tide as I indicated?
> > > > > >
> > > > > > Alkaline substances raise pH. That is their nature because they bind
> > > > > > up H+ protons reducing their concentration.
> > > > > >
> > > > > Yes but how antacids effects internally in blood?
> > > >
> > > > It reacts to reduce the concentration of H+ protons.
> > > >
> > > On absorption or otherwise?
> >
> > Chemical reaction with a base.
> >
> On excessive intake of antacids, whether these are absorbed in blood or
> not?

No.

> If no, how these can act as base and raise blood and urine pH?

In typically don't when taken in the usual dosages.

> > > > > > > > > Furthur, can it be possible that insulin esp.long term, if injected in
> > > > > > > > > fat tissues don't reach to blood?
> > > > > > > >
> > > > > > > > No.
> > > > > > > >
> > > > > > > > > If yes, what can resist it except
> > > > > > > > > distance? Can there be some defects by excess fats or some fatty
> > > > > > > > > degeneration and scarring alike in liver Cirrhosis which may interfere
> > > > > > > > > in insulin transport?
> > > > > > > >
> > > > > > > > No.
> > > > > > > >
> > > > > > > What does it mean that it can become non-physyological in fats?
> > > > > >
> > > > > > It does not mean anything. Fats are physiological.
> > > > > >
> > > > > You told insulin can be non-physiological in fats. What does it mean?
> > > >
> > > > Local environments within adipose tissue compartments can be rendered
> > > > nonphysiological for extended periods of time without affecting
> > > > homeostasis of the vascular compartment.
> > > >
> > > By local environment you mean normal or altered?
> >
> > Either.
> >
> Do You mean Local environments within adipose tissue compartments can
> be rendered
> nonphysiological for extended periods of time in general or will ir be
> nonphysiological just for insulin?

The former.

> > > Will then insulin be degraded ?
> >
> > No.
> >
> Will then injected insulin as such in fats, be stored for extended
> periods of time?

Not stored but released more slowly.

> If yes, can it be release excessively sometimes in
> blood?

Typically not.

> > > Can fatty degerations
> > > are possible other than in liver and heart?
> >
> > You probably mean fatty infiltration.
> >
> Yes and damages done by such fatty infilterations. I think it is now
> called as fatty changes. Whether any imbalance in K or in sulphur
> containing protien cause fatty infiltrations and fatty degenarations?

No.

> One, Potassium sulphate based healing agent in one alt. system is
> indicated for fatty degenarations. It is also indicated for uremia. Can
> there be some link between it with fatty infiltrations and elevated
> BUN?

No.

> > > If yes, which are other
> > > parts?
> >
> > Pancreas and spleen can also have fatty infiltration.
> >
> Muscles and testis?

Yes.

Will be available to "glow" and chat about this and other things like
cardiology, diabetes, cooking and nutrition that interest those
following this thread here during the next on-line chat (02/09/06) from
6 to 7 pm EST:

http://tinyurl.com/cpayh

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

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/8juld
 
Andrew B. Chung, MD/PhD wrote:
> Kumar wrote:
> > Andrew B. Chung, MD/PhD wrote:
> > > Kumar wrote:
> > > > > > Can't elevated lactic acid damage tissue?
> > > > >
> > > > > Not under physiological conditions.
> > > > >
> > > > Can elevated lactic acid at any part cause pain in that part?
> > >
> > > Not under physiological conditions.
> > >
> > How anyone get pain on any inflammation?
>
> Through the stimulation of the nerve endings of pain fibers.
>
What are the stimuli for the stimulation of the nerve endings of pain
fibers?

> > > > > > Can't tissue before damage be
> > > > > > treated alike Exercising/exerting muscles resulting into lactate
> > > > > > accumulation and some acidosis effect?
> > > > >
> > > > > Yes.
> > > > > > > > > Not under physiological conditions.
> > > > > > > > How these raise serum pH--by absorption of antacids or by opposte
> > > > > > > > effect due to more secretion of HCl to neutralize antacids in stomach
> > > > > > > > or by alkaline tide as I indicated?
> > > > > > >
> > > > > > > Alkaline substances raise pH. That is their nature because they bind
> > > > > > > up H+ protons reducing their concentration.
> > > > > > >
> > > > > > Yes but how antacids effects internally in blood?
> > > > >
> > > > > It reacts to reduce the concentration of H+ protons.
> > > > >
> > > > On absorption or otherwise?
> > >
> > > Chemical reaction with a base.
> > >
> > On excessive intake of antacids, whether these are absorbed in blood or
> > not?
>
> No.
>
> > If no, how these can act as base and raise blood and urine pH?
>
> In typically don't when taken in the usual dosages.
Yes, but when antacids are not absorbed in blood, how antacids, when
taken in excess quantity can raise pH of blood & urine?
>
> > > > > > > > > > Furthur, can it be possible that insulin esp.long term, if injected in
> > > > > > > > > > fat tissues don't reach to blood?
> > > > > > > > >
> > > > > > > > > No.
> > > > > > > > >
> > > > > > > > > > If yes, what can resist it except
> > > > > > > > > > distance? Can there be some defects by excess fats or some fatty
> > > > > > > > > > degeneration and scarring alike in liver Cirrhosis which may interfere
> > > > > > > > > > in insulin transport?
> > > > > > > > >
> > > > > > > > > No.
> > > > > > > > >
> > > > > > > > What does it mean that it can become non-physyological in fats?
> > > > > > >
> > > > > > > It does not mean anything. Fats are physiological.
> > > > > > >
> > > > > > You told insulin can be non-physiological in fats. What does it mean?
> > > > >
> > > > > Local environments within adipose tissue compartments can be rendered
> > > > > nonphysiological for extended periods of time without affecting
> > > > > homeostasis of the vascular compartment.
> > > > >
> > > > By local environment you mean normal or altered?
> > >
> > > Either.
> > >
> > Do You mean Local environments within adipose tissue compartments can
> > be rendered
> > nonphysiological for extended periods of time in general or will ir be
> > nonphysiological just for insulin?
>
> The former.

Can there be some other reasons of persisting of hyperglycemia than
overeating, Insulin resistance, visc..adoposity, insufficient medicines
or insulin intake, low needle size, insulin slow transport due to fats
esp. long acting, stress, inflammations and infections?

How persistent elevated glucose in blood is directly harmful
(non-elevated lipids related)? Can it accumulate somewhere or cause
toxicity to any tissues directly?

Glucose atract water, so water retention in blood can be possible due
to elevated sugar levels resulting change in tonicity. It may cause
cells to take more water and swell. Can this happen, if yes, what can
be its results?
 
Kumar wrote:
> Andrew B. Chung, MD/PhD wrote:
> > Kumar wrote:
> > > Andrew B. Chung, MD/PhD wrote:
> > > > Kumar wrote:
> > > > > > > Can't elevated lactic acid damage tissue?
> > > > > >
> > > > > > Not under physiological conditions.
> > > > > >
> > > > > Can elevated lactic acid at any part cause pain in that part?
> > > >
> > > > Not under physiological conditions.
> > > >
> > > How anyone get pain on any inflammation?
> >
> > Through the stimulation of the nerve endings of pain fibers.
> >
> What are the stimuli for the stimulation of the nerve endings of pain
> fibers?

Nonphysiological conditions.

> > > > > > > Can't tissue before damage be
> > > > > > > treated alike Exercising/exerting muscles resulting into lactate
> > > > > > > accumulation and some acidosis effect?
> > > > > >
> > > > > > Yes.
> > > > > > > > > > Not under physiological conditions.
> > > > > > > > > How these raise serum pH--by absorption of antacids or by opposte
> > > > > > > > > effect due to more secretion of HCl to neutralize antacids in stomach
> > > > > > > > > or by alkaline tide as I indicated?
> > > > > > > >
> > > > > > > > Alkaline substances raise pH. That is their nature because they bind
> > > > > > > > up H+ protons reducing their concentration.
> > > > > > > >
> > > > > > > Yes but how antacids effects internally in blood?
> > > > > >
> > > > > > It reacts to reduce the concentration of H+ protons.
> > > > > >
> > > > > On absorption or otherwise?
> > > >
> > > > Chemical reaction with a base.
> > > >
> > > On excessive intake of antacids, whether these are absorbed in blood or
> > > not?
> >
> > No.
> >
> > > If no, how these can act as base and raise blood and urine pH?
> >
> > In typically don't when taken in the usual dosages.
> Yes, but when antacids are not absorbed in blood, how antacids, when
> taken in excess quantity can raise pH of blood & urine?

The stomach's production of gastric acid to overcome the antacid
becomes much greater than the amount of bicarbonate released into the
small intestine to neutralize mash coming from the stomach.

> > > > > > > > > > > Furthur, can it be possible that insulin esp.long term, if injected in
> > > > > > > > > > > fat tissues don't reach to blood?
> > > > > > > > > >
> > > > > > > > > > No.
> > > > > > > > > >
> > > > > > > > > > > If yes, what can resist it except
> > > > > > > > > > > distance? Can there be some defects by excess fats or some fatty
> > > > > > > > > > > degeneration and scarring alike in liver Cirrhosis which may interfere
> > > > > > > > > > > in insulin transport?
> > > > > > > > > >
> > > > > > > > > > No.
> > > > > > > > > >
> > > > > > > > > What does it mean that it can become non-physyological in fats?
> > > > > > > >
> > > > > > > > It does not mean anything. Fats are physiological.
> > > > > > > >
> > > > > > > You told insulin can be non-physiological in fats. What does it mean?
> > > > > >
> > > > > > Local environments within adipose tissue compartments can be rendered
> > > > > > nonphysiological for extended periods of time without affecting
> > > > > > homeostasis of the vascular compartment.
> > > > > >
> > > > > By local environment you mean normal or altered?
> > > >
> > > > Either.
> > > >
> > > Do You mean Local environments within adipose tissue compartments can
> > > be rendered
> > > nonphysiological for extended periods of time in general or will ir be
> > > nonphysiological just for insulin?
> >
> > The former.
>
> Can there be some other reasons of persisting of hyperglycemia than
> overeating, Insulin resistance, visc..adoposity, insufficient medicines
> or insulin intake, low needle size, insulin slow transport due to fats
> esp. long acting, stress, inflammations and infections?

Yes.

> How persistent elevated glucose in blood is directly harmful
> (non-elevated lipids related)?

It results in the glycosylation of structural proteins.

> Can it accumulate somewhere or cause
> toxicity to any tissues directly?

The latter.

> Glucose atract water, so water retention in blood can be possible due
> to elevated sugar levels resulting change in tonicity. It may cause
> cells to take more water and swell. Can this happen, if yes, what can
> be its results?

Does not happen in practice.

Will be available to "glow" and chat about this and other things like
cardiology, diabetes, cooking and nutrition that interest those
following this thread here during the next on-line chat (02/09/06) from
6 to 7 pm EST:

http://tinyurl.com/cpayh

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

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/8juld
 
Andrew B. Chung, MD/PhD wrote:
> Kumar wrote:
> > Andrew B. Chung, MD/PhD wrote:
> > > Kumar wrote:
> > > > Andrew B. Chung, MD/PhD wrote:
> > > > > Kumar wrote:
> > > > > > > > Can't elevated lactic acid damage tissue?
> > > > > > >
> > > > > > > Not under physiological conditions.
> > > > > > >
> > > > > > Can elevated lactic acid at any part cause pain in that part?
> > > > >
> > > > > Not under physiological conditions.
> > > > >
> > > > How anyone get pain on any inflammation?
> > >
> > > Through the stimulation of the nerve endings of pain fibers.
> > >
> > What are the stimuli for the stimulation of the nerve endings of pain
> > fibers?
>
> Nonphysiological conditions.
>
> > > > > > > > Can't tissue before damage be
> > > > > > > > treated alike Exercising/exerting muscles resulting into lactate
> > > > > > > > accumulation and some acidosis effect?
> > > > > > >
> > > > > > > Yes.
> > > > > > > > > > > Not under physiological conditions.
> > > > > > > > > > How these raise serum pH--by absorption of antacids or by opposte
> > > > > > > > > > effect due to more secretion of HCl to neutralize antacids in stomach
> > > > > > > > > > or by alkaline tide as I indicated?
> > > > > > > > >
> > > > > > > > > Alkaline substances raise pH. That is their nature because they bind
> > > > > > > > > up H+ protons reducing their concentration.
> > > > > > > > >
> > > > > > > > Yes but how antacids effects internally in blood?
> > > > > > >
> > > > > > > It reacts to reduce the concentration of H+ protons.
> > > > > > >
> > > > > > On absorption or otherwise?
> > > > >
> > > > > Chemical reaction with a base.
> > > > >
> > > > On excessive intake of antacids, whether these are absorbed in blood or
> > > > not?
> > >
> > > No.
> > >
> > > > If no, how these can act as base and raise blood and urine pH?
> > >
> > > In typically don't when taken in the usual dosages.
> > Yes, but when antacids are not absorbed in blood, how antacids, when
> > taken in excess quantity can raise pH of blood & urine?
>
> The stomach's production of gastric acid to overcome the antacid
> becomes much greater than the amount of bicarbonate released into the
> small intestine to neutralize mash coming from the stomach.
>
How then it will raise pH of blood or of urine?

> > > > > > > > > > > > Furthur, can it be possible that insulin esp.long term, if injected in
> > > > > > > > > > > > fat tissues don't reach to blood?
> > > > > > > > > > >
> > > > > > > > > > > No.
> > > > > > > > > > >
> > > > > > > > > > > > If yes, what can resist it except
> > > > > > > > > > > > distance? Can there be some defects by excess fats or some fatty
> > > > > > > > > > > > degeneration and scarring alike in liver Cirrhosis which may interfere
> > > > > > > > > > > > in insulin transport?
> > > > > > > > > > >
> > > > > > > > > > > No.
> > > > > > > > > > >
> > > > > > > > > > What does it mean that it can become non-physyological in fats?
> > > > > > > > >
> > > > > > > > > It does not mean anything. Fats are physiological.
> > > > > > > > >
> > > > > > > > You told insulin can be non-physiological in fats. What does it mean?
> > > > > > >
> > > > > > > Local environments within adipose tissue compartments can be rendered
> > > > > > > nonphysiological for extended periods of time without affecting
> > > > > > > homeostasis of the vascular compartment.
> > > > > > >
> > > > > > By local environment you mean normal or altered?
> > > > >
> > > > > Either.
> > > > >
> > > > Do You mean Local environments within adipose tissue compartments can
> > > > be rendered
> > > > nonphysiological for extended periods of time in general or will ir be
> > > > nonphysiological just for insulin?
> > >
> > > The former.
> >
Can there be differances in fats tissues and in their densities or gaps
in extracellular spaces betwwen differant people? I mean can fat
tissues be more premble in one whereas lesser in others? Actually, it
appears that, injected insulin esp. long acting is very much effective
in few people whereas lesser in others inspite they look equally fat?

> > Can there be some other reasons of persisting of hyperglycemia than
> > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > or insulin intake, low needle size, insulin slow transport due to fats
> > esp. long acting, stress, inflammations and infections?
>
> Yes.
>
I think acidosis is left. What are other reasons?

> > How persistent elevated glucose in blood is directly harmful
> > (non-elevated lipids related)?
>
> It results in the glycosylation of structural proteins.
>
Thanks. Rest I will check.
I think it also increases chances of some infections esp. in urinary
tract?
> > Can it accumulate somewhere or cause

> > toxicity to any tissues directly?
>
> The latter.
>
> > Glucose atract water, so water retention in blood can be possible due
> > to elevated sugar levels resulting change in tonicity. It may cause
> > cells to take more water and swell. Can this happen, if yes, what can
> > be its results?
>
> Does not happen in practice.

Btw can elevated glucose levels have some benefits also?
>
> Will be available to "glow" and chat about this and other things like
> cardiology, diabetes, cooking and nutrition that interest those
> following this thread here during the next on-line chat (02/09/06) from
> 6 to 7 pm EST:
>
> http://tinyurl.com/cpayh
>
> For those who are put off by the signature, my advance apologies for
> how the LORD has reshaped me:
>
> http://tinyurl.com/bgfqt
>
> Prayerfully in Christ's love,
>
> Andrew
> http://tinyurl.com/8juld
 
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:
> > > > > > > > > Can't elevated lactic acid damage tissue?
> > > > > > > >
> > > > > > > > Not under physiological conditions.
> > > > > > > >
> > > > > > > Can elevated lactic acid at any part cause pain in that part?
> > > > > >
> > > > > > Not under physiological conditions.
> > > > > >
> > > > > How anyone get pain on any inflammation?
> > > >
> > > > Through the stimulation of the nerve endings of pain fibers.
> > > >
> > > What are the stimuli for the stimulation of the nerve endings of pain
> > > fibers?
> >
> > Nonphysiological conditions.
> >
> > > > > > > > > Can't tissue before damage be
> > > > > > > > > treated alike Exercising/exerting muscles resulting into lactate
> > > > > > > > > accumulation and some acidosis effect?
> > > > > > > >
> > > > > > > > Yes.
> > > > > > > > > > > > Not under physiological conditions.
> > > > > > > > > > > How these raise serum pH--by absorption of antacids or by opposte
> > > > > > > > > > > effect due to more secretion of HCl to neutralize antacids in stomach
> > > > > > > > > > > or by alkaline tide as I indicated?
> > > > > > > > > >
> > > > > > > > > > Alkaline substances raise pH. That is their nature because they bind
> > > > > > > > > > up H+ protons reducing their concentration.
> > > > > > > > > >
> > > > > > > > > Yes but how antacids effects internally in blood?
> > > > > > > >
> > > > > > > > It reacts to reduce the concentration of H+ protons.
> > > > > > > >
> > > > > > > On absorption or otherwise?
> > > > > >
> > > > > > Chemical reaction with a base.
> > > > > >
> > > > > On excessive intake of antacids, whether these are absorbed in blood or
> > > > > not?
> > > >
> > > > No.
> > > >
> > > > > If no, how these can act as base and raise blood and urine pH?
> > > >
> > > > In typically don't when taken in the usual dosages.
> > > Yes, but when antacids are not absorbed in blood, how antacids, when
> > > taken in excess quantity can raise pH of blood & urine?
> >
> > The stomach's production of gastric acid to overcome the antacid
> > becomes much greater than the amount of bicarbonate released into the
> > small intestine to neutralize mash coming from the stomach.
> >
> How then it will raise pH of blood or of urine?

By lowering the concentration of H+ protons.

> > > > > > > > > > > > > Furthur, can it be possible that insulin esp.long term, if injected in
> > > > > > > > > > > > > fat tissues don't reach to blood?
> > > > > > > > > > > >
> > > > > > > > > > > > No.
> > > > > > > > > > > >
> > > > > > > > > > > > > If yes, what can resist it except
> > > > > > > > > > > > > distance? Can there be some defects by excess fats or some fatty
> > > > > > > > > > > > > degeneration and scarring alike in liver Cirrhosis which may interfere
> > > > > > > > > > > > > in insulin transport?
> > > > > > > > > > > >
> > > > > > > > > > > > No.
> > > > > > > > > > > >
> > > > > > > > > > > What does it mean that it can become non-physyological in fats?
> > > > > > > > > >
> > > > > > > > > > It does not mean anything. Fats are physiological.
> > > > > > > > > >
> > > > > > > > > You told insulin can be non-physiological in fats. What does it mean?
> > > > > > > >
> > > > > > > > Local environments within adipose tissue compartments can be rendered
> > > > > > > > nonphysiological for extended periods of time without affecting
> > > > > > > > homeostasis of the vascular compartment.
> > > > > > > >
> > > > > > > By local environment you mean normal or altered?
> > > > > >
> > > > > > Either.
> > > > > >
> > > > > Do You mean Local environments within adipose tissue compartments can
> > > > > be rendered
> > > > > nonphysiological for extended periods of time in general or will ir be
> > > > > nonphysiological just for insulin?
> > > >
> > > > The former.
> > >
> Can there be differances in fats tissues and in their densities or gaps
> in extracellular spaces betwwen differant people?

Yes.

> I mean can fat
> tissues be more premble in one whereas lesser in others?

Yes.

> Actually, it
> appears that, injected insulin esp. long acting is very much effective
> in few people whereas lesser in others inspite they look equally fat?

We are each individually and wonderfully made by the LORD.

> > > Can there be some other reasons of persisting of hyperglycemia than
> > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > or insulin intake, low needle size, insulin slow transport due to fats
> > > esp. long acting, stress, inflammations and infections?
> >
> > Yes.
> >
> I think acidosis is left. What are other reasons?

Hormonal derangements.

> > > How persistent elevated glucose in blood is directly harmful
> > > (non-elevated lipids related)?
> >
> > It results in the glycosylation of structural proteins.
> >
> Thanks. Rest I will check.
> I think it also increases chances of some infections esp. in urinary
> tract?

Yes.

> > > Can it accumulate somewhere or cause
>
> > > toxicity to any tissues directly?
> >
> > The latter.
> >
> > > Glucose atract water, so water retention in blood can be possible due
> > > to elevated sugar levels resulting change in tonicity. It may cause
> > > cells to take more water and swell. Can this happen, if yes, what can
> > > be its results?
> >
> > Does not happen in practice.
>
> Btw can elevated glucose levels have some benefits also?

Fuel for muscles.

Will be available to "glow" and chat about this and other things like
cardiology, diabetes, BIrd Flu, cooking and nutrition that interest
those following this thread here during the next on-line chat
(02/09/06) from 6 to 7 pm EST:

http://tinyurl.com/cpayh

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

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/8juld
 
Andrew B. Chung, MD/PhD wrote:
> Kumar wrote:
> > > The stomach's production of gastric acid to overcome the antacid
> > > becomes much greater than the amount of bicarbonate released into the
> > > small intestine to neutralize mash coming from the stomach.
> > >
> > How then it will raise pH of blood or of urine?
>
> By lowering the concentration of H+ protons.
>
> > > > > > > > > > > > > > Furthur, can it be possible that insulin esp.long term, if injected in
> > > > > > > > > > > > > > fat tissues don't reach to blood?
> > > > > > > > > > > > >
> > > > > > > > > > > > > No.
> > > > > > > > > > > > >
> > > > > > > > > > > > > > If yes, what can resist it except
> > > > > > > > > > > > > > distance? Can there be some defects by excess fats or some fatty
> > > > > > > > > > > > > > degeneration and scarring alike in liver Cirrhosis which may interfere
> > > > > > > > > > > > > > in insulin transport?
> > > > > > > > > > > > >
> > > > > > > > > > > > > No.
> > > > > > > > > > > > >
> > > > > > > > > > > > What does it mean that it can become non-physyological in fats?
> > > > > > > > > > >
> > > > > > > > > > > It does not mean anything. Fats are physiological.
> > > > > > > > > > >
> > > > > > > > > > You told insulin can be non-physiological in fats. What does it mean?
> > > > > > > > >
> > > > > > > > > Local environments within adipose tissue compartments can be rendered
> > > > > > > > > nonphysiological for extended periods of time without affecting
> > > > > > > > > homeostasis of the vascular compartment.
> > > > > > > > >
> > > > > > > > By local environment you mean normal or altered?
> > > > > > >
> > > > > > > Either.
> > > > > > >
> > > > > > Do You mean Local environments within adipose tissue compartments can
> > > > > > be rendered
> > > > > > nonphysiological for extended periods of time in general or will ir be
> > > > > > nonphysiological just for insulin?
> > > > >
> > > > > The former.
> > > >
> > Can there be differances in fats tissues and in their densities or gaps
> > in extracellular spaces betwwen differant people?
>
> Yes.
>
> > I mean can fat
> > tissues be more premble in one whereas lesser in others?
>
> Yes.
>
> > Actually, it
> > appears that, injected insulin esp. long acting is very much effective
> > in few people whereas lesser in others inspite they look equally fat?
>
> We are each individually and wonderfully made by the LORD.

Yes, but con. system don't have "constitutions medicines" based on
individuality and disease type? Many system consider this concept
primarily.

> > > > Can there be some other reasons of persisting of hyperglycemia than
> > > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > > or insulin intake, low needle size, insulin slow transport due to fats
> > > > esp. long acting, stress, inflammations and infections?
> > >
> > > Yes.
> > >
> > I think acidosis is left. What are other reasons?
>
> Hormonal derangements.
>
Oh, "dark under the lamp" .Will it be only insulin derangements? If no,
which are other?

> > > > How persistent elevated glucose in blood is directly harmful
> > > > (non-elevated lipids related)?
> > >
> > > It results in the glycosylation of structural proteins.
> > >
> > Thanks. Rest I will check.
> > I think it also increases chances of some infections esp. in urinary
> > tract?
>
> Yes.
>
Whether increasing pH of digestive tract, blood, urine or of
reproductive parts by medications or foods can result comparatively
more infections?
> > > > Can it accumulate somewhere or cause
> >
> > > > toxicity to any tissues directly?
> > >
> > > The latter.
> > >
> > > > Glucose atract water, so water retention in blood can be possible due
> > > > to elevated sugar levels resulting change in tonicity. It may cause
> > > > cells to take more water and swell. Can this happen, if yes, what can
> > > > be its results?
> > >
> > > Does not happen in practice.
> >
> > Btw can elevated glucose levels have some benefits also?
>
> Fuel for muscles.

Any other?

It looks, LORD has given me more "questions" and to you more/most
"awnsers".
May LORD bless.
 
Kumar wrote:
>
> Andrew B. Chung, MD/PhD wrote:
> > Kumar wrote:
> > > > The stomach's production of gastric acid to overcome the antacid
> > > > becomes much greater than the amount of bicarbonate released into the
> > > > small intestine to neutralize mash coming from the stomach.
> > > >
> > > How then it will raise pH of blood or of urine?
> >
> > By lowering the concentration of H+ protons.
> >
> > > > > > > > > > > > > > > Furthur, can it be possible that insulin esp.long term, if injected in
> > > > > > > > > > > > > > > fat tissues don't reach to blood?
> > > > > > > > > > > > > >
> > > > > > > > > > > > > > No.
> > > > > > > > > > > > > >
> > > > > > > > > > > > > > > If yes, what can resist it except
> > > > > > > > > > > > > > > distance? Can there be some defects by excess fats or some fatty
> > > > > > > > > > > > > > > degeneration and scarring alike in liver Cirrhosis which may interfere
> > > > > > > > > > > > > > > in insulin transport?
> > > > > > > > > > > > > >
> > > > > > > > > > > > > > No.
> > > > > > > > > > > > > >
> > > > > > > > > > > > > What does it mean that it can become non-physyological in fats?
> > > > > > > > > > > >
> > > > > > > > > > > > It does not mean anything. Fats are physiological.
> > > > > > > > > > > >
> > > > > > > > > > > You told insulin can be non-physiological in fats. What does it mean?
> > > > > > > > > >
> > > > > > > > > > Local environments within adipose tissue compartments can be rendered
> > > > > > > > > > nonphysiological for extended periods of time without affecting
> > > > > > > > > > homeostasis of the vascular compartment.
> > > > > > > > > >
> > > > > > > > > By local environment you mean normal or altered?
> > > > > > > >
> > > > > > > > Either.
> > > > > > > >
> > > > > > > Do You mean Local environments within adipose tissue compartments can
> > > > > > > be rendered
> > > > > > > nonphysiological for extended periods of time in general or will ir be
> > > > > > > nonphysiological just for insulin?
> > > > > >
> > > > > > The former.
> > > > >
> > > Can there be differances in fats tissues and in their densities or gaps
> > > in extracellular spaces betwwen differant people?
> >
> > Yes.
> >
> > > I mean can fat
> > > tissues be more premble in one whereas lesser in others?
> >
> > Yes.
> >
> > > Actually, it
> > > appears that, injected insulin esp. long acting is very much effective
> > > in few people whereas lesser in others inspite they look equally fat?
> >
> > We are each individually and wonderfully made by the LORD.
>
> Yes, but con. system don't have "constitutions medicines" based on
> individuality and disease type? Many system consider this concept
> primarily.

This will have to be determined empirically.

> > > > > Can there be some other reasons of persisting of hyperglycemia than
> > > > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > > > or insulin intake, low needle size, insulin slow transport due to fats
> > > > > esp. long acting, stress, inflammations and infections?
> > > >
> > > > Yes.
> > > >
> > > I think acidosis is left. What are other reasons?
> >
> > Hormonal derangements.
> >
> Oh, "dark under the lamp" .Will it be only insulin derangements? If no,
> which are other?

One example would be glucocorticoid excess.

> > > > > How persistent elevated glucose in blood is directly harmful
> > > > > (non-elevated lipids related)?
> > > >
> > > > It results in the glycosylation of structural proteins.
> > > >
> > > Thanks. Rest I will check.
> > > I think it also increases chances of some infections esp. in urinary
> > > tract?
> >
> > Yes.
> >
> Whether increasing pH of digestive tract, blood, urine or of
> reproductive parts by medications or foods can result comparatively
> more infections?

Not typically.

> > > > > Can it accumulate somewhere or cause
> > >
> > > > > toxicity to any tissues directly?
> > > >
> > > > The latter.
> > > >
> > > > > Glucose atract water, so water retention in blood can be possible due
> > > > > to elevated sugar levels resulting change in tonicity. It may cause
> > > > > cells to take more water and swell. Can this happen, if yes, what can
> > > > > be its results?
> > > >
> > > > Does not happen in practice.
> > >
> > > Btw can elevated glucose levels have some benefits also?
> >
> > Fuel for muscles.
>
> Any other?

Not really.

> It looks, LORD has given me more "questions" and to you more/most
> "awnsers".
> May LORD bless.

Thank you for your kind thoughts and thank the LORD for HIS continued
blessings.

Will be available to "glow" and chat about this and other things like
cardiology, diabetes, Bird Flu, cooking and nutrition that interest
those following this thread here during the next on-line chat (02/09/06)
from 6 to 7 pm EST:

http://tinyurl.com/cpayh

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

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/8juld
 
Andrew B. Chung, MD/PhD wrote:
> Kumar wrote:
>> > > We are each individually and wonderfully made by the LORD.
> >
> > Yes, but con. system don't have "constitutions medicines" based on
> > individuality and disease type? Many system consider this concept
> > primarily.
>
> This will have to be determined empirically.
>
Can't be people, diseases and medicines be classified as per acis, base
and water imbalances?

I think that different people have predisposed and persistent tendancy
to any of these imbalances.

> > > > > > Can there be some other reasons of persisting of hyperglycemia than
> > > > > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > > > > or insulin intake, low needle size, insulin slow transport due to fats
> > > > > > esp. long acting, stress, inflammations and infections?
> > > > >
> > > > > Yes.
> > > > >
> > > > I think acidosis is left. What are other reasons?
> > >
> > > Hormonal derangements.
> > >
> > Oh, "dark under the lamp" .Will it be only insulin derangements? If no,
> > which are other?
>
> One example would be glucocorticoid excess.

Any other example?
>
> > > > > > How persistent elevated glucose in blood is directly harmful
> > > > > > (non-elevated lipids related)?
> > > > >
> > > > > It results in the glycosylation of structural proteins.
> > > > >


""Endogenous glycations occur mainly in the bloodstream to a small
proportion of the absorbed simple sugars: glucose, fructose and
galactose. The balance of the sugar molecules are used for metabolic
processes. It appears that fructose and galactose have approximately
ten times the glycation activity of glucose, the primary body fuel
(McPherson et al 1988). Glycation is the first step in the evolution of
these molecules through a complex series of very slow reactions in the
body known as Amadori reactions, Schiff base reactions, and Maillard
reactions; all lead to advanced glycation endproducts (AGEs). Some AGEs
are benign, but others are more reactive than the sugars they are
derived from, and are implicated in many age-related chronic diseases
such as: type II diabetes mellitus (beta cell damage), cardiovascular
diseases (the endothelium and collagen are damaged), Alzheimer's
disease (amyloid proteins are side products of the reactions
progressing to AGEs), cancer (acrylamide and other side products are
released), peripheral neuropathy (the myelin is attacked), and other
sensory losses such as deafness (due to demyelination) and blindness
(mostly due to microvascular damage in the retina). This range of
diseases is the result of the very basic level at which glycations
interfere with molecular and cellular functioning throughout the body
and the release of highly oxidizing side products such as hydrogen
peroxide.

Glycated substances are eliminated from the body slowly, since the
renal clearance factor is only about 30%. This implies that the half
life of a glycation within the body is about double the average cell
life. Red blood cells are the shortest lived cells in the body (120
days), so, the half life is about 240 days. This fact is used in
monitoring blood sugar control in diabetes by monitoring the glycated
hemoglobin level. Consequently, long lived cells (such as nerves, brain
cells,) and long lasting proteins (such as DNA, eye crystalline, and
collagen) may accumulate substantial damage over time. Metabolically
active cells such as the glomeruli in the kidneys, retina cells in the
eyes, and beta cells (insulin producing) in the pancreas are also at
high risk of damage. The epithelial cells of the blood vessels are
damaged directly by glycations, which are implicated in
atherosclerosis, for example. Atherosclerotic plaque tends to
accumulate at areas of high blood flow (such as the entrance to the
coronary arteries) due to the increased presentation of sugar
molecules, glycations and glycation end products at these points.
Damage by glycation results in stiffening of the collagen in the blood
vessel walls leading to high blood pressure. Glycations also cause
weakening of the collagen in the blood vessel walls, which may lead to
micro- or macro aneurisms; this may cause strokes if in the brain.""
http://en.wikipedia.org/wiki/Glycation

"The sugar group can assist in protein folding or improve its
stability. Glycoproteins are often used in proteins that are at least
in part located in extracellular space (that is, outside the cell)."

"Experiments have shown that glycosylation in this case is not a strict
requirement for proper folding, but the unglycosylated protein degrades
quickly. Glycosylation may play a role in cell-cell adhesion""

How hyperglycemia effected Glycosylation and glycation of proteins or
Glycoproteins can cause persistent elevated glucose level, insulin
resistance, damge to beta cells in pacreas and complications related
with diabetes?
 
Kumar wrote:
> Andrew B. Chung, MD/PhD wrote:
> > Kumar wrote:
> >> > > We are each individually and wonderfully made by the LORD.
> > >
> > > Yes, but con. system don't have "constitutions medicines" based on
> > > individuality and disease type? Many system consider this concept
> > > primarily.
> >
> > This will have to be determined empirically.
> >
> Can't be people, diseases and medicines be classified as per acis, base
> and water imbalances?

No.

> I think that different people have predisposed and persistent tendancy
> to any of these imbalances.

That is not what we see.

> > > > > > > Can there be some other reasons of persisting of hyperglycemia than
> > > > > > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > > > > > or insulin intake, low needle size, insulin slow transport due to fats
> > > > > > > esp. long acting, stress, inflammations and infections?
> > > > > >
> > > > > > Yes.
> > > > > >
> > > > > I think acidosis is left. What are other reasons?
> > > >
> > > > Hormonal derangements.
> > > >
> > > Oh, "dark under the lamp" .Will it be only insulin derangements? If no,
> > > which are other?
> >
> > One example would be glucocorticoid excess.
>
> Any other example?

Yes. Glucagon excess.

> > > > > > > How persistent elevated glucose in blood is directly harmful
> > > > > > > (non-elevated lipids related)?
> > > > > >
> > > > > > It results in the glycosylation of structural proteins.
> > > > > >
>
>
> ""Endogenous glycations occur mainly in the bloodstream to a small
> proportion of the absorbed simple sugars: glucose, fructose and
> galactose. The balance of the sugar molecules are used for metabolic
> processes. It appears that fructose and galactose have approximately
> ten times the glycation activity of glucose, the primary body fuel
> (McPherson et al 1988). Glycation is the first step in the evolution of
> these molecules through a complex series of very slow reactions in the
> body known as Amadori reactions, Schiff base reactions, and Maillard
> reactions; all lead to advanced glycation endproducts (AGEs). Some AGEs
> are benign, but others are more reactive than the sugars they are
> derived from, and are implicated in many age-related chronic diseases
> such as: type II diabetes mellitus (beta cell damage), cardiovascular
> diseases (the endothelium and collagen are damaged), Alzheimer's
> disease (amyloid proteins are side products of the reactions
> progressing to AGEs), cancer (acrylamide and other side products are
> released), peripheral neuropathy (the myelin is attacked), and other
> sensory losses such as deafness (due to demyelination) and blindness
> (mostly due to microvascular damage in the retina). This range of
> diseases is the result of the very basic level at which glycations
> interfere with molecular and cellular functioning throughout the body
> and the release of highly oxidizing side products such as hydrogen
> peroxide.
>
> Glycated substances are eliminated from the body slowly, since the
> renal clearance factor is only about 30%. This implies that the half
> life of a glycation within the body is about double the average cell
> life. Red blood cells are the shortest lived cells in the body (120
> days), so, the half life is about 240 days. This fact is used in
> monitoring blood sugar control in diabetes by monitoring the glycated
> hemoglobin level. Consequently, long lived cells (such as nerves, brain
> cells,) and long lasting proteins (such as DNA, eye crystalline, and
> collagen) may accumulate substantial damage over time. Metabolically
> active cells such as the glomeruli in the kidneys, retina cells in the
> eyes, and beta cells (insulin producing) in the pancreas are also at
> high risk of damage. The epithelial cells of the blood vessels are
> damaged directly by glycations, which are implicated in
> atherosclerosis, for example. Atherosclerotic plaque tends to
> accumulate at areas of high blood flow (such as the entrance to the
> coronary arteries) due to the increased presentation of sugar
> molecules, glycations and glycation end products at these points.
> Damage by glycation results in stiffening of the collagen in the blood
> vessel walls leading to high blood pressure. Glycations also cause
> weakening of the collagen in the blood vessel walls, which may lead to
> micro- or macro aneurisms; this may cause strokes if in the brain.""
> http://en.wikipedia.org/wiki/Glycation
>
> "The sugar group can assist in protein folding or improve its
> stability. Glycoproteins are often used in proteins that are at least
> in part located in extracellular space (that is, outside the cell)."
>
> "Experiments have shown that glycosylation in this case is not a strict
> requirement for proper folding, but the unglycosylated protein degrades
> quickly. Glycosylation may play a role in cell-cell adhesion""
>
> How hyperglycemia effected Glycosylation and glycation of proteins or
> Glycoproteins can cause persistent elevated glucose level, insulin
> resistance, damge to beta cells in pacreas and complications related
> with diabetes?

Your question has been answered by what you have cited.

Will be available to "glow" and chat about this and other things like
cardiology, diabetes, Bird Flu, cooking and nutrition that interest
those following this thread here during the next on-line chat
(02/09/06) from 6 to 7 pm EST:

http://tinyurl.com/cpayh

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

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/8juld
 
Andrew B. Chung, MD/PhD wrote:
> Kumar wrote:
> > Andrew B. Chung, MD/PhD wrote:
> > > Kumar wrote:
> > >> > > We are each individually and wonderfully made by the LORD.
> > > >
> > > > Yes, but con. system don't have "constitutions medicines" based on
> > > > individuality and disease type? Many system consider this concept
> > > > primarily.
> > >
> > > This will have to be determined empirically.
> > >
> > Can't be people, diseases and medicines be classified as per acis, base
> > and water imbalances?
>
> No.
>
> > I think that different people have predisposed and persistent tendancy
> > to any of these imbalances.
>
> That is not what we see.
>
> > > > > > > > Can there be some other reasons of persisting of hyperglycemia than
> > > > > > > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > > > > > > or insulin intake, low needle size, insulin slow transport due to fats
> > > > > > > > esp. long acting, stress, inflammations and infections?
> > > > > > >
> > > > > > > Yes.
> > > > > > >
> > > > > > I think acidosis is left. What are other reasons?
> > > > >
> > > > > Hormonal derangements.
> > > > >
> > > > Oh, "dark under the lamp" .Will it be only insulin derangements? If no,
> > > > which are other?
> > >
> > > One example would be glucocorticoid excess.
> >
> > Any other example?
>
> Yes. Glucagon excess.
>
Yes, some more?
> > > > > > > > How persistent elevated glucose in blood is directly harmful
> > > > > > > > (non-elevated lipids related)?
> > > > > > >
> > > > > > > It results in the glycosylation of structural proteins.
> > > > > > >
> >
> >
> > ""Endogenous glycations occur mainly in the bloodstream to a small
> > proportion of the absorbed simple sugars: glucose, fructose and
> > galactose. The balance of the sugar molecules are used for metabolic
> > processes. It appears that fructose and galactose have approximately
> > ten times the glycation activity of glucose, the primary body fuel
> > (McPherson et al 1988). Glycation is the first step in the evolution of
> > these molecules through a complex series of very slow reactions in the
> > body known as Amadori reactions, Schiff base reactions, and Maillard
> > reactions; all lead to advanced glycation endproducts (AGEs). Some AGEs
> > are benign, but others are more reactive than the sugars they are
> > derived from, and are implicated in many age-related chronic diseases
> > such as: type II diabetes mellitus (beta cell damage), cardiovascular
> > diseases (the endothelium and collagen are damaged), Alzheimer's
> > disease (amyloid proteins are side products of the reactions
> > progressing to AGEs), cancer (acrylamide and other side products are
> > released), peripheral neuropathy (the myelin is attacked), and other
> > sensory losses such as deafness (due to demyelination) and blindness
> > (mostly due to microvascular damage in the retina). This range of
> > diseases is the result of the very basic level at which glycations
> > interfere with molecular and cellular functioning throughout the body
> > and the release of highly oxidizing side products such as hydrogen
> > peroxide.
> >
> > Glycated substances are eliminated from the body slowly, since the
> > renal clearance factor is only about 30%. This implies that the half
> > life of a glycation within the body is about double the average cell
> > life. Red blood cells are the shortest lived cells in the body (120
> > days), so, the half life is about 240 days. This fact is used in
> > monitoring blood sugar control in diabetes by monitoring the glycated
> > hemoglobin level. Consequently, long lived cells (such as nerves, brain
> > cells,) and long lasting proteins (such as DNA, eye crystalline, and
> > collagen) may accumulate substantial damage over time. Metabolically
> > active cells such as the glomeruli in the kidneys, retina cells in the
> > eyes, and beta cells (insulin producing) in the pancreas are also at
> > high risk of damage. The epithelial cells of the blood vessels are
> > damaged directly by glycations, which are implicated in
> > atherosclerosis, for example. Atherosclerotic plaque tends to
> > accumulate at areas of high blood flow (such as the entrance to the
> > coronary arteries) due to the increased presentation of sugar
> > molecules, glycations and glycation end products at these points.
> > Damage by glycation results in stiffening of the collagen in the blood
> > vessel walls leading to high blood pressure. Glycations also cause
> > weakening of the collagen in the blood vessel walls, which may lead to
> > micro- or macro aneurisms; this may cause strokes if in the brain.""
> > http://en.wikipedia.org/wiki/Glycation
> >
> > "The sugar group can assist in protein folding or improve its
> > stability. Glycoproteins are often used in proteins that are at least
> > in part located in extracellular space (that is, outside the cell)."
> >
> > "Experiments have shown that glycosylation in this case is not a strict
> > requirement for proper folding, but the unglycosylated protein degrades
> > quickly. Glycosylation may play a role in cell-cell adhesion""
> >
> > How hyperglycemia effected Glycosylation and glycation of proteins or
> > Glycoproteins can cause persistent elevated glucose level, insulin
> > resistance, damge to beta cells in pacreas and complications related
> > with diabetes?
>
> Your question has been answered by what you have cited.

It is not clear to me that how Glycosylation and glycation can effect
insulin effectiveness as insulin is also a protien? Whether glycation
and Glycosylation can increase stability and prevent degradation of
insulin--mean if can increase insulin's effectiveness?
 
Kumar wrote:
> Andrew B. Chung, MD/PhD wrote:
> > Kumar wrote:
> > > Andrew B. Chung, MD/PhD wrote:
> > > > Kumar wrote:
> > > >> > > We are each individually and wonderfully made by the LORD.
> > > > >
> > > > > Yes, but con. system don't have "constitutions medicines" based on
> > > > > individuality and disease type? Many system consider this concept
> > > > > primarily.
> > > >
> > > > This will have to be determined empirically.
> > > >
> > > Can't be people, diseases and medicines be classified as per acis, base
> > > and water imbalances?
> >
> > No.
> >
> > > I think that different people have predisposed and persistent tendancy
> > > to any of these imbalances.
> >
> > That is not what we see.
> >
> > > > > > > > > Can there be some other reasons of persisting of hyperglycemia than
> > > > > > > > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > > > > > > > or insulin intake, low needle size, insulin slow transport due to fats
> > > > > > > > > esp. long acting, stress, inflammations and infections?
> > > > > > > >
> > > > > > > > Yes.
> > > > > > > >
> > > > > > > I think acidosis is left. What are other reasons?
> > > > > >
> > > > > > Hormonal derangements.
> > > > > >
> > > > > Oh, "dark under the lamp" .Will it be only insulin derangements? If no,
> > > > > which are other?
> > > >
> > > > One example would be glucocorticoid excess.
> > >
> > > Any other example?
> >
> > Yes. Glucagon excess.
>
> Yes, some more?

Growth hormone deficiency.

> > > > > > > > > How persistent elevated glucose in blood is directly harmful
> > > > > > > > > (non-elevated lipids related)?
> > > > > > > >
> > > > > > > > It results in the glycosylation of structural proteins.
> > > > > > > >
> > >
> > >
> > > ""Endogenous glycations occur mainly in the bloodstream to a small
> > > proportion of the absorbed simple sugars: glucose, fructose and
> > > galactose. The balance of the sugar molecules are used for metabolic
> > > processes. It appears that fructose and galactose have approximately
> > > ten times the glycation activity of glucose, the primary body fuel
> > > (McPherson et al 1988). Glycation is the first step in the evolution of
> > > these molecules through a complex series of very slow reactions in the
> > > body known as Amadori reactions, Schiff base reactions, and Maillard
> > > reactions; all lead to advanced glycation endproducts (AGEs). Some AGEs
> > > are benign, but others are more reactive than the sugars they are
> > > derived from, and are implicated in many age-related chronic diseases
> > > such as: type II diabetes mellitus (beta cell damage), cardiovascular
> > > diseases (the endothelium and collagen are damaged), Alzheimer's
> > > disease (amyloid proteins are side products of the reactions
> > > progressing to AGEs), cancer (acrylamide and other side products are
> > > released), peripheral neuropathy (the myelin is attacked), and other
> > > sensory losses such as deafness (due to demyelination) and blindness
> > > (mostly due to microvascular damage in the retina). This range of
> > > diseases is the result of the very basic level at which glycations
> > > interfere with molecular and cellular functioning throughout the body
> > > and the release of highly oxidizing side products such as hydrogen
> > > peroxide.
> > >
> > > Glycated substances are eliminated from the body slowly, since the
> > > renal clearance factor is only about 30%. This implies that the half
> > > life of a glycation within the body is about double the average cell
> > > life. Red blood cells are the shortest lived cells in the body (120
> > > days), so, the half life is about 240 days. This fact is used in
> > > monitoring blood sugar control in diabetes by monitoring the glycated
> > > hemoglobin level. Consequently, long lived cells (such as nerves, brain
> > > cells,) and long lasting proteins (such as DNA, eye crystalline, and
> > > collagen) may accumulate substantial damage over time. Metabolically
> > > active cells such as the glomeruli in the kidneys, retina cells in the
> > > eyes, and beta cells (insulin producing) in the pancreas are also at
> > > high risk of damage. The epithelial cells of the blood vessels are
> > > damaged directly by glycations, which are implicated in
> > > atherosclerosis, for example. Atherosclerotic plaque tends to
> > > accumulate at areas of high blood flow (such as the entrance to the
> > > coronary arteries) due to the increased presentation of sugar
> > > molecules, glycations and glycation end products at these points.
> > > Damage by glycation results in stiffening of the collagen in the blood
> > > vessel walls leading to high blood pressure. Glycations also cause
> > > weakening of the collagen in the blood vessel walls, which may lead to
> > > micro- or macro aneurisms; this may cause strokes if in the brain.""
> > > http://en.wikipedia.org/wiki/Glycation
> > >
> > > "The sugar group can assist in protein folding or improve its
> > > stability. Glycoproteins are often used in proteins that are at least
> > > in part located in extracellular space (that is, outside the cell)."
> > >
> > > "Experiments have shown that glycosylation in this case is not a strict
> > > requirement for proper folding, but the unglycosylated protein degrades
> > > quickly. Glycosylation may play a role in cell-cell adhesion""
> > >
> > > How hyperglycemia effected Glycosylation and glycation of proteins or
> > > Glycoproteins can cause persistent elevated glucose level, insulin
> > > resistance, damge to beta cells in pacreas and complications related
> > > with diabetes?
> >
> > Your question has been answered by what you have cited.
>
> It is not clear to me that how Glycosylation and glycation can effect
> insulin effectiveness as insulin is also a protien?

The beta cells are made up of many proteins that function less
optimally when glycated.

> Whether glycation
> and Glycosylation can increase stability and prevent degradation of
> insulin--mean if can increase insulin's effectiveness?

Insulin is not altered by elevated serum glucose.

Will be available to "glow" and chat about this and other things like
cardiology, diabetes, Bird Flu, cooking and nutrition that interest
those following this thread here during the next on-line chat
(02/09/06) from 6 to 7 pm EST:

http://tinyurl.com/8w7uq

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

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/8juld
 
Andrew B. Chung, MD/PhD wrote:
> Kumar wrote:
> > Andrew B. Chung, MD/PhD wrote:
> > > Kumar wrote:
> > > > Andrew B. Chung, MD/PhD wrote:
> > > > > Kumar wrote:
> > > > >> > > We are each individually and wonderfully made by the LORD.
> > > > > >
> > > > > > Yes, but con. system don't have "constitutions medicines" based on
> > > > > > individuality and disease type? Many system consider this concept
> > > > > > primarily.
> > > > >
> > > > > This will have to be determined empirically.
> > > > >
> > > > Can't be people, diseases and medicines be classified as per acis, base
> > > > and water imbalances?
> > >
> > > No.
> > >
> > > > I think that different people have predisposed and persistent tendancy
> > > > to any of these imbalances.
> > >
> > > That is not what we see.
> > >
> > > > > > > > > > Can there be some other reasons of persisting of hyperglycemia than
> > > > > > > > > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > > > > > > > > or insulin intake, low needle size, insulin slow transport due to fats
> > > > > > > > > > esp. long acting, stress, inflammations and infections?
> > > > > > > > >
> > > > > > > > > Yes.
> > > > > > > > >
> > > > > > > > I think acidosis is left. What are other reasons?
> > > > > > >
> > > > > > > Hormonal derangements.
> > > > > > >
> > > > > > Oh, "dark under the lamp" .Will it be only insulin derangements? If no,
> > > > > > which are other?
> > > > >
> > > > > One example would be glucocorticoid excess.
> > > >
> > > > Any other example?
> > >
> > > Yes. Glucagon excess.
> >
> > Yes, some more?
>
> Growth hormone deficiency.
>
Some more? Pls tell all in one shot.

> > > > > > > > > > How persistent elevated glucose in blood is directly harmful
> > > > > > > > > > (non-elevated lipids related)?
> > > > > > > > >
> > > > > > > > > It results in the glycosylation of structural proteins.
> > > > > > > > >
> > > >
> > > >
> > > > ""Endogenous glycations occur mainly in the bloodstream to a small
> > > > proportion of the absorbed simple sugars: glucose, fructose and
> > > > galactose. The balance of the sugar molecules are used for metabolic
> > > > processes. It appears that fructose and galactose have approximately
> > > > ten times the glycation activity of glucose, the primary body fuel
> > > > (McPherson et al 1988). Glycation is the first step in the evolution of
> > > > these molecules through a complex series of very slow reactions in the
> > > > body known as Amadori reactions, Schiff base reactions, and Maillard
> > > > reactions; all lead to advanced glycation endproducts (AGEs). Some AGEs
> > > > are benign, but others are more reactive than the sugars they are
> > > > derived from, and are implicated in many age-related chronic diseases
> > > > such as: type II diabetes mellitus (beta cell damage), cardiovascular
> > > > diseases (the endothelium and collagen are damaged), Alzheimer's
> > > > disease (amyloid proteins are side products of the reactions
> > > > progressing to AGEs), cancer (acrylamide and other side products are
> > > > released), peripheral neuropathy (the myelin is attacked), and other
> > > > sensory losses such as deafness (due to demyelination) and blindness
> > > > (mostly due to microvascular damage in the retina). This range of
> > > > diseases is the result of the very basic level at which glycations
> > > > interfere with molecular and cellular functioning throughout the body
> > > > and the release of highly oxidizing side products such as hydrogen
> > > > peroxide.
> > > >
> > > > Glycated substances are eliminated from the body slowly, since the
> > > > renal clearance factor is only about 30%. This implies that the half
> > > > life of a glycation within the body is about double the average cell
> > > > life. Red blood cells are the shortest lived cells in the body (120
> > > > days), so, the half life is about 240 days. This fact is used in
> > > > monitoring blood sugar control in diabetes by monitoring the glycated
> > > > hemoglobin level. Consequently, long lived cells (such as nerves, brain
> > > > cells,) and long lasting proteins (such as DNA, eye crystalline, and
> > > > collagen) may accumulate substantial damage over time. Metabolically
> > > > active cells such as the glomeruli in the kidneys, retina cells in the
> > > > eyes, and beta cells (insulin producing) in the pancreas are also at
> > > > high risk of damage. The epithelial cells of the blood vessels are
> > > > damaged directly by glycations, which are implicated in
> > > > atherosclerosis, for example. Atherosclerotic plaque tends to
> > > > accumulate at areas of high blood flow (such as the entrance to the
> > > > coronary arteries) due to the increased presentation of sugar
> > > > molecules, glycations and glycation end products at these points.
> > > > Damage by glycation results in stiffening of the collagen in the blood
> > > > vessel walls leading to high blood pressure. Glycations also cause
> > > > weakening of the collagen in the blood vessel walls, which may lead to
> > > > micro- or macro aneurisms; this may cause strokes if in the brain.""
> > > > http://en.wikipedia.org/wiki/Glycation
> > > >
> > > > "The sugar group can assist in protein folding or improve its
> > > > stability. Glycoproteins are often used in proteins that are at least
> > > > in part located in extracellular space (that is, outside the cell)."
> > > >
> > > > "Experiments have shown that glycosylation in this case is not a strict
> > > > requirement for proper folding, but the unglycosylated protein degrades
> > > > quickly. Glycosylation may play a role in cell-cell adhesion""
> > > >
> > > > How hyperglycemia effected Glycosylation and glycation of proteins or
> > > > Glycoproteins can cause persistent elevated glucose level, insulin
> > > > resistance, damge to beta cells in pacreas and complications related
> > > > with diabetes?
> > >
> > > Your question has been answered by what you have cited.
> >
> > It is not clear to me that how Glycosylation and glycation can effect
> > insulin effectiveness as insulin is also a protien?
>
> The beta cells are made up of many proteins that function less
> optimally when glycated.
>
Means, beta cells will produce less insulin when glycated?


> > Whether glycation
> > and Glycosylation can increase stability and prevent degradation of
> > insulin--mean if can increase insulin's effectiveness?
>
> Insulin is not altered by elevated serum glucose.

What about detachment of C-peptide in view of glycation and
Glycosylation can increase stability and prevent degradation of
protiens?
 
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:
> > > > > >> > > We are each individually and wonderfully made by the LORD.
> > > > > > >
> > > > > > > Yes, but con. system don't have "constitutions medicines" based on
> > > > > > > individuality and disease type? Many system consider this concept
> > > > > > > primarily.
> > > > > >
> > > > > > This will have to be determined empirically.
> > > > > >
> > > > > Can't be people, diseases and medicines be classified as per acis, base
> > > > > and water imbalances?
> > > >
> > > > No.
> > > >
> > > > > I think that different people have predisposed and persistent tendancy
> > > > > to any of these imbalances.
> > > >
> > > > That is not what we see.
> > > >
> > > > > > > > > > > Can there be some other reasons of persisting of hyperglycemia than
> > > > > > > > > > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > > > > > > > > > or insulin intake, low needle size, insulin slow transport due to fats
> > > > > > > > > > > esp. long acting, stress, inflammations and infections?
> > > > > > > > > >
> > > > > > > > > > Yes.
> > > > > > > > > >
> > > > > > > > > I think acidosis is left. What are other reasons?
> > > > > > > >
> > > > > > > > Hormonal derangements.
> > > > > > > >
> > > > > > > Oh, "dark under the lamp" .Will it be only insulin derangements? If no,
> > > > > > > which are other?
> > > > > >
> > > > > > One example would be glucocorticoid excess.
> > > > >
> > > > > Any other example?
> > > >
> > > > Yes. Glucagon excess.
> > >
> > > Yes, some more?
> >
> > Growth hormone deficiency.
> >
> Some more? Pls tell all in one shot.

Elevations in any steroid hormone has the potential for causing
hyperglycemia.

> > > > > > > > > > > How persistent elevated glucose in blood is directly harmful
> > > > > > > > > > > (non-elevated lipids related)?
> > > > > > > > > >
> > > > > > > > > > It results in the glycosylation of structural proteins.
> > > > > > > > > >
> > > > >
> > > > >
> > > > > ""Endogenous glycations occur mainly in the bloodstream to a small
> > > > > proportion of the absorbed simple sugars: glucose, fructose and
> > > > > galactose. The balance of the sugar molecules are used for metabolic
> > > > > processes. It appears that fructose and galactose have approximately
> > > > > ten times the glycation activity of glucose, the primary body fuel
> > > > > (McPherson et al 1988). Glycation is the first step in the evolution of
> > > > > these molecules through a complex series of very slow reactions in the
> > > > > body known as Amadori reactions, Schiff base reactions, and Maillard
> > > > > reactions; all lead to advanced glycation endproducts (AGEs). Some AGEs
> > > > > are benign, but others are more reactive than the sugars they are
> > > > > derived from, and are implicated in many age-related chronic diseases
> > > > > such as: type II diabetes mellitus (beta cell damage), cardiovascular
> > > > > diseases (the endothelium and collagen are damaged), Alzheimer's
> > > > > disease (amyloid proteins are side products of the reactions
> > > > > progressing to AGEs), cancer (acrylamide and other side products are
> > > > > released), peripheral neuropathy (the myelin is attacked), and other
> > > > > sensory losses such as deafness (due to demyelination) and blindness
> > > > > (mostly due to microvascular damage in the retina). This range of
> > > > > diseases is the result of the very basic level at which glycations
> > > > > interfere with molecular and cellular functioning throughout the body
> > > > > and the release of highly oxidizing side products such as hydrogen
> > > > > peroxide.
> > > > >
> > > > > Glycated substances are eliminated from the body slowly, since the
> > > > > renal clearance factor is only about 30%. This implies that the half
> > > > > life of a glycation within the body is about double the average cell
> > > > > life. Red blood cells are the shortest lived cells in the body (120
> > > > > days), so, the half life is about 240 days. This fact is used in
> > > > > monitoring blood sugar control in diabetes by monitoring the glycated
> > > > > hemoglobin level. Consequently, long lived cells (such as nerves, brain
> > > > > cells,) and long lasting proteins (such as DNA, eye crystalline, and
> > > > > collagen) may accumulate substantial damage over time. Metabolically
> > > > > active cells such as the glomeruli in the kidneys, retina cells in the
> > > > > eyes, and beta cells (insulin producing) in the pancreas are also at
> > > > > high risk of damage. The epithelial cells of the blood vessels are
> > > > > damaged directly by glycations, which are implicated in
> > > > > atherosclerosis, for example. Atherosclerotic plaque tends to
> > > > > accumulate at areas of high blood flow (such as the entrance to the
> > > > > coronary arteries) due to the increased presentation of sugar
> > > > > molecules, glycations and glycation end products at these points.
> > > > > Damage by glycation results in stiffening of the collagen in the blood
> > > > > vessel walls leading to high blood pressure. Glycations also cause
> > > > > weakening of the collagen in the blood vessel walls, which may lead to
> > > > > micro- or macro aneurisms; this may cause strokes if in the brain.""
> > > > > http://en.wikipedia.org/wiki/Glycation
> > > > >
> > > > > "The sugar group can assist in protein folding or improve its
> > > > > stability. Glycoproteins are often used in proteins that are at least
> > > > > in part located in extracellular space (that is, outside the cell)."
> > > > >
> > > > > "Experiments have shown that glycosylation in this case is not a strict
> > > > > requirement for proper folding, but the unglycosylated protein degrades
> > > > > quickly. Glycosylation may play a role in cell-cell adhesion""
> > > > >
> > > > > How hyperglycemia effected Glycosylation and glycation of proteins or
> > > > > Glycoproteins can cause persistent elevated glucose level, insulin
> > > > > resistance, damge to beta cells in pacreas and complications related
> > > > > with diabetes?
> > > >
> > > > Your question has been answered by what you have cited.
> > >
> > > It is not clear to me that how Glycosylation and glycation can effect
> > > insulin effectiveness as insulin is also a protien?
> >
> > The beta cells are made up of many proteins that function less
> > optimally when glycated.
> >
> Means, beta cells will produce less insulin when glycated?

Yes. This is the pathophysiology of glucotoxicity.

> > > Whether glycation
> > > and Glycosylation can increase stability and prevent degradation of
> > > insulin--mean if can increase insulin's effectiveness?
> >
> > Insulin is not altered by elevated serum glucose.
>
> What about detachment of C-peptide in view of glycation and
> Glycosylation can increase stability and prevent degradation of
> protiens?

Not for insulin.

Will be available to "glow" and chat about this and other things like
cardiology, diabetes, Bird Flu, cooking and nutrition that interest
those following this thread here during the next on-line chat
(02/16/06) from 6 to 7 pm EST:

http://tinyurl.com/cpayh

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

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/8juld
 
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:
> > > > > > >> > > We are each individually and wonderfully made by the LORD.
> > > > > > > >
> > > > > > > > Yes, but con. system don't have "constitutions medicines" based on
> > > > > > > > individuality and disease type? Many system consider this concept
> > > > > > > > primarily.
> > > > > > >
> > > > > > > This will have to be determined empirically.
> > > > > > >
> > > > > > Can't be people, diseases and medicines be classified as per acis, base
> > > > > > and water imbalances?
> > > > >
> > > > > No.
> > > > >
> > > > > > I think that different people have predisposed and persistent tendancy
> > > > > > to any of these imbalances.
> > > > >
> > > > > That is not what we see.
> > > > >
> > > > > > > > > > > > Can there be some other reasons of persisting of hyperglycemia than
> > > > > > > > > > > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > > > > > > > > > > or insulin intake, low needle size, insulin slow transport due to fats
> > > > > > > > > > > > esp. long acting, stress, inflammations and infections?
> > > > > > > > > > >
> > > > > > > > > > > Yes.
> > > > > > > > > > >
> > > > > > > > > > I think acidosis is left. What are other reasons?
> > > > > > > > >
> > > > > > > > > Hormonal derangements.
> > > > > > > > >
> > > > > > > > Oh, "dark under the lamp" .Will it be only insulin derangements? If no,
> > > > > > > > which are other?
> > > > > > >
> > > > > > > One example would be glucocorticoid excess.
> > > > > >
> > > > > > Any other example?
> > > > >
> > > > > Yes. Glucagon excess.
> > > >
> > > > Yes, some more?
> > >
> > > Growth hormone deficiency.
> > >
> > Some more? Pls tell all in one shot.
>
> Elevations in any steroid hormone has the potential for causing
> hyperglycemia.

Thanks. You may tell if anyone is left.
> > > > > > > > > > > > How persistent elevated glucose in blood is directly harmful
> > > > > > > > > > > > (non-elevated lipids related)?
> > > > > > > > > > >
> > > > > > > > > > > It results in the glycosylation of structural proteins.
> > > > > > > > > > >
> > > > > >
> > > > > >
> > > > > > ""Endogenous glycations occur mainly in the bloodstream to a small
> > > > > > proportion of the absorbed simple sugars: glucose, fructose and
> > > > > > galactose. The balance of the sugar molecules are used for metabolic
> > > > > > processes. It appears that fructose and galactose have approximately
> > > > > > ten times the glycation activity of glucose, the primary body fuel
> > > > > > (McPherson et al 1988). Glycation is the first step in the evolution of
> > > > > > these molecules through a complex series of very slow reactions in the
> > > > > > body known as Amadori reactions, Schiff base reactions, and Maillard
> > > > > > reactions; all lead to advanced glycation endproducts (AGEs). Some AGEs
> > > > > > are benign, but others are more reactive than the sugars they are
> > > > > > derived from, and are implicated in many age-related chronic diseases
> > > > > > such as: type II diabetes mellitus (beta cell damage), cardiovascular
> > > > > > diseases (the endothelium and collagen are damaged), Alzheimer's
> > > > > > disease (amyloid proteins are side products of the reactions
> > > > > > progressing to AGEs), cancer (acrylamide and other side products are
> > > > > > released), peripheral neuropathy (the myelin is attacked), and other
> > > > > > sensory losses such as deafness (due to demyelination) and blindness
> > > > > > (mostly due to microvascular damage in the retina). This range of
> > > > > > diseases is the result of the very basic level at which glycations
> > > > > > interfere with molecular and cellular functioning throughout the body
> > > > > > and the release of highly oxidizing side products such as hydrogen
> > > > > > peroxide.
> > > > > >
> > > > > > Glycated substances are eliminated from the body slowly, since the
> > > > > > renal clearance factor is only about 30%. This implies that the half
> > > > > > life of a glycation within the body is about double the average cell
> > > > > > life. Red blood cells are the shortest lived cells in the body (120
> > > > > > days), so, the half life is about 240 days. This fact is used in
> > > > > > monitoring blood sugar control in diabetes by monitoring the glycated
> > > > > > hemoglobin level. Consequently, long lived cells (such as nerves, brain
> > > > > > cells,) and long lasting proteins (such as DNA, eye crystalline, and
> > > > > > collagen) may accumulate substantial damage over time. Metabolically
> > > > > > active cells such as the glomeruli in the kidneys, retina cells in the
> > > > > > eyes, and beta cells (insulin producing) in the pancreas are also at
> > > > > > high risk of damage. The epithelial cells of the blood vessels are
> > > > > > damaged directly by glycations, which are implicated in
> > > > > > atherosclerosis, for example. Atherosclerotic plaque tends to
> > > > > > accumulate at areas of high blood flow (such as the entrance to the
> > > > > > coronary arteries) due to the increased presentation of sugar
> > > > > > molecules, glycations and glycation end products at these points.
> > > > > > Damage by glycation results in stiffening of the collagen in the blood
> > > > > > vessel walls leading to high blood pressure. Glycations also cause
> > > > > > weakening of the collagen in the blood vessel walls, which may lead to
> > > > > > micro- or macro aneurisms; this may cause strokes if in the brain.""
> > > > > > http://en.wikipedia.org/wiki/Glycation
> > > > > >
> > > > > > "The sugar group can assist in protein folding or improve its
> > > > > > stability. Glycoproteins are often used in proteins that are at least
> > > > > > in part located in extracellular space (that is, outside the cell)."
> > > > > >
> > > > > > "Experiments have shown that glycosylation in this case is not a strict
> > > > > > requirement for proper folding, but the unglycosylated protein degrades
> > > > > > quickly. Glycosylation may play a role in cell-cell adhesion""
> > > > > >
> > > > > > How hyperglycemia effected Glycosylation and glycation of proteins or
> > > > > > Glycoproteins can cause persistent elevated glucose level, insulin
> > > > > > resistance, damge to beta cells in pacreas and complications related
> > > > > > with diabetes?
> > > > >
> > > > > Your question has been answered by what you have cited.
> > > >
> > > > It is not clear to me that how Glycosylation and glycation can effect
> > > > insulin effectiveness as insulin is also a protien?
> > >
> > > The beta cells are made up of many proteins that function less
> > > optimally when glycated.
> > >
> > Means, beta cells will produce less insulin when glycated?
>
> Yes. This is the pathophysiology of glucotoxicity.
>
Sorry but elevated glucose level causes more secretion of insulin?
> > > > Whether glycation
> > > > and Glycosylation can increase stability and prevent degradation of
> > > > insulin--mean if can increase insulin's effectiveness?
> > >
> > > Insulin is not altered by elevated serum glucose.
> >
> > What about detachment of C-peptide in view of glycation and
> > Glycosylation can increase stability and prevent degradation of
> > protiens?
>
> Not for insulin.

Any other secondary effect, by which insulin secretion is effected due
to glycation or glycosylation ?
 
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:
> > > > > > > Andrew B. Chung, MD/PhD wrote:
> > > > > > > > Kumar wrote:
> > > > > > > >> > > We are each individually and wonderfully made by the LORD.
> > > > > > > > >
> > > > > > > > > Yes, but con. system don't have "constitutions medicines" based on
> > > > > > > > > individuality and disease type? Many system consider this concept
> > > > > > > > > primarily.
> > > > > > > >
> > > > > > > > This will have to be determined empirically.
> > > > > > > >
> > > > > > > Can't be people, diseases and medicines be classified as per acis, base
> > > > > > > and water imbalances?
> > > > > >
> > > > > > No.
> > > > > >
> > > > > > > I think that different people have predisposed and persistent tendancy
> > > > > > > to any of these imbalances.
> > > > > >
> > > > > > That is not what we see.
> > > > > >
> > > > > > > > > > > > > Can there be some other reasons of persisting of hyperglycemia than
> > > > > > > > > > > > > overeating, Insulin resistance, visc..adoposity, insufficient medicines
> > > > > > > > > > > > > or insulin intake, low needle size, insulin slow transport due to fats
> > > > > > > > > > > > > esp. long acting, stress, inflammations and infections?
> > > > > > > > > > > >
> > > > > > > > > > > > Yes.
> > > > > > > > > > > >
> > > > > > > > > > > I think acidosis is left. What are other reasons?
> > > > > > > > > >
> > > > > > > > > > Hormonal derangements.
> > > > > > > > > >
> > > > > > > > > Oh, "dark under the lamp" .Will it be only insulin derangements? If no,
> > > > > > > > > which are other?
> > > > > > > >
> > > > > > > > One example would be glucocorticoid excess.
> > > > > > >
> > > > > > > Any other example?
> > > > > >
> > > > > > Yes. Glucagon excess.
> > > > >
> > > > > Yes, some more?
> > > >
> > > > Growth hormone deficiency.
> > > >
> > > Some more? Pls tell all in one shot.
> >
> > Elevations in any steroid hormone has the potential for causing
> > hyperglycemia.
>
> Thanks. You may tell if anyone is left.

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

> > > > > > > > > > > > > How persistent elevated glucose in blood is directly harmful
> > > > > > > > > > > > > (non-elevated lipids related)?
> > > > > > > > > > > >
> > > > > > > > > > > > It results in the glycosylation of structural proteins.
> > > > > > > > > > > >
> > > > > > >
> > > > > > >
> > > > > > > ""Endogenous glycations occur mainly in the bloodstream to a small
> > > > > > > proportion of the absorbed simple sugars: glucose, fructose and
> > > > > > > galactose. The balance of the sugar molecules are used for metabolic
> > > > > > > processes. It appears that fructose and galactose have approximately
> > > > > > > ten times the glycation activity of glucose, the primary body fuel
> > > > > > > (McPherson et al 1988). Glycation is the first step in the evolution of
> > > > > > > these molecules through a complex series of very slow reactions in the
> > > > > > > body known as Amadori reactions, Schiff base reactions, and Maillard
> > > > > > > reactions; all lead to advanced glycation endproducts (AGEs). Some AGEs
> > > > > > > are benign, but others are more reactive than the sugars they are
> > > > > > > derived from, and are implicated in many age-related chronic diseases
> > > > > > > such as: type II diabetes mellitus (beta cell damage), cardiovascular
> > > > > > > diseases (the endothelium and collagen are damaged), Alzheimer's
> > > > > > > disease (amyloid proteins are side products of the reactions
> > > > > > > progressing to AGEs), cancer (acrylamide and other side products are
> > > > > > > released), peripheral neuropathy (the myelin is attacked), and other
> > > > > > > sensory losses such as deafness (due to demyelination) and blindness
> > > > > > > (mostly due to microvascular damage in the retina). This range of
> > > > > > > diseases is the result of the very basic level at which glycations
> > > > > > > interfere with molecular and cellular functioning throughout the body
> > > > > > > and the release of highly oxidizing side products such as hydrogen
> > > > > > > peroxide.
> > > > > > >
> > > > > > > Glycated substances are eliminated from the body slowly, since the
> > > > > > > renal clearance factor is only about 30%. This implies that the half
> > > > > > > life of a glycation within the body is about double the average cell
> > > > > > > life. Red blood cells are the shortest lived cells in the body (120
> > > > > > > days), so, the half life is about 240 days. This fact is used in
> > > > > > > monitoring blood sugar control in diabetes by monitoring the glycated
> > > > > > > hemoglobin level. Consequently, long lived cells (such as nerves, brain
> > > > > > > cells,) and long lasting proteins (such as DNA, eye crystalline, and
> > > > > > > collagen) may accumulate substantial damage over time. Metabolically
> > > > > > > active cells such as the glomeruli in the kidneys, retina cells in the
> > > > > > > eyes, and beta cells (insulin producing) in the pancreas are also at
> > > > > > > high risk of damage. The epithelial cells of the blood vessels are
> > > > > > > damaged directly by glycations, which are implicated in
> > > > > > > atherosclerosis, for example. Atherosclerotic plaque tends to
> > > > > > > accumulate at areas of high blood flow (such as the entrance to the
> > > > > > > coronary arteries) due to the increased presentation of sugar
> > > > > > > molecules, glycations and glycation end products at these points.
> > > > > > > Damage by glycation results in stiffening of the collagen in the blood
> > > > > > > vessel walls leading to high blood pressure. Glycations also cause
> > > > > > > weakening of the collagen in the blood vessel walls, which may lead to
> > > > > > > micro- or macro aneurisms; this may cause strokes if in the brain.""
> > > > > > > http://en.wikipedia.org/wiki/Glycation
> > > > > > >
> > > > > > > "The sugar group can assist in protein folding or improve its
> > > > > > > stability. Glycoproteins are often used in proteins that are at least
> > > > > > > in part located in extracellular space (that is, outside the cell)."
> > > > > > >
> > > > > > > "Experiments have shown that glycosylation in this case is not a strict
> > > > > > > requirement for proper folding, but the unglycosylated protein degrades
> > > > > > > quickly. Glycosylation may play a role in cell-cell adhesion""
> > > > > > >
> > > > > > > How hyperglycemia effected Glycosylation and glycation of proteins or
> > > > > > > Glycoproteins can cause persistent elevated glucose level, insulin
> > > > > > > resistance, damge to beta cells in pacreas and complications related
> > > > > > > with diabetes?
> > > > > >
> > > > > > Your question has been answered by what you have cited.
> > > > >
> > > > > It is not clear to me that how Glycosylation and glycation can effect
> > > > > insulin effectiveness as insulin is also a protien?
> > > >
> > > > The beta cells are made up of many proteins that function less
> > > > optimally when glycated.
> > > >
> > > Means, beta cells will produce less insulin when glycated?
> >
> > Yes. This is the pathophysiology of glucotoxicity.
> >
> Sorry but elevated glucose level causes more secretion of insulin?

It does until the beta cells become glucotoxic.

> > > > > Whether glycation
> > > > > and Glycosylation can increase stability and prevent degradation of
> > > > > insulin--mean if can increase insulin's effectiveness?
> > > >
> > > > Insulin is not altered by elevated serum glucose.
> > >
> > > What about detachment of C-peptide in view of glycation and
> > > Glycosylation can increase stability and prevent degradation of
> > > protiens?
> >
> > Not for insulin.
>
> Any other secondary effect, by which insulin secretion is effected due
> to glycation or glycosylation ?

See above.

Will be available to "glow" and chat about this and other things like
cardiology, diabetes, Bird Flu, cooking and nutrition that interest
those following this thread here during the next on-line chat (02/16/06)
from 6 to 7 pm EST:

http://tinyurl.com/8w7uq

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

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/8juld
 
Andrew B. Chung, MD/PhD wrote:
> kumar wrote:
> > > > > >
> > > > > > It is not clear to me that how Glycosylation and glycation can effect
> > > > > > insulin effectiveness as insulin is also a protien?
> > > > >
> > > > > The beta cells are made up of many proteins that function less
> > > > > optimally when glycated.
> > > > >
> > > > Means, beta cells will produce less insulin when glycated?
> > >
> > > Yes. This is the pathophysiology of glucotoxicity.
> > >
> > Sorry but elevated glucose level causes more secretion of insulin?
>
> It does until the beta cells become glucotoxic.
>
Is there any logic behind beta cells damage due to glucotoxicity?
Logically, body mechanism should protect and regenrate more beta cells
on gulucotoxicity?

Once damaged, whether beta cells don't regenerate?


Does it take long time with persisting hyperglycemia for cells to
become gulucotoxic? If yes, appx. how much?
> > > > What about detachment of C-peptide in view of glycation and
> > > > Glycosylation can increase stability and prevent degradation of
> > > > protiens?
> > >
> > > Not for insulin.
> >
Which other type of cells effected by glucotoxicity?
 
Kumar wrote:
> Andrew B. Chung, MD/PhD wrote:
> > kumar wrote:
> > > > > > >
> > > > > > > It is not clear to me that how Glycosylation and glycation can effect
> > > > > > > insulin effectiveness as insulin is also a protien?
> > > > > >
> > > > > > The beta cells are made up of many proteins that function less
> > > > > > optimally when glycated.
> > > > > >
> > > > > Means, beta cells will produce less insulin when glycated?
> > > >
> > > > Yes. This is the pathophysiology of glucotoxicity.
> > > >
> > > Sorry but elevated glucose level causes more secretion of insulin?
> >
> > It does until the beta cells become glucotoxic.
> >
> Is there any logic behind beta cells damage due to glucotoxicity?

No.

> Logically, body mechanism should protect and regenrate more beta cells
> on gulucotoxicity?

Such is the penalty for overeating.

> Once damaged, whether beta cells don't regenerate?

They can recover.

> Does it take long time with persisting hyperglycemia for cells to
> become gulucotoxic?

No.

> If yes, appx. how much?

It does not take a long time.

> > > > > What about detachment of C-peptide in view of glycation and
> > > > > Glycosylation can increase stability and prevent degradation of
> > > > > protiens?
> > > >
> > > > Not for insulin.
> > >
> Which other type of cells effected by glucotoxicity?

All are.

Will be available to "glow" and chat about this and other things like
cardiology, diabetes, Bird Flu, cooking and nutrition that interest
those following this thread here during the next on-line chat
(02/16/06) from 6 to 7 pm EST:

http://tinyurl.com/8w7uq

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

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/8juld
 
Andrew B. Chung, MD/PhD wrote:
> Kumar wrote:
> > Andrew B. Chung, MD/PhD wrote:
> > > kumar wrote:
> > > > > > > >
> > > > > > > > It is not clear to me that how Glycosylation and glycation can effect
> > > > > > > > insulin effectiveness as insulin is also a protien?
> > > > > > >
> > > > > > > The beta cells are made up of many proteins that function less
> > > > > > > optimally when glycated.
> > > > > > >
> > > > > > Means, beta cells will produce less insulin when glycated?
> > > > >
> > > > > Yes. This is the pathophysiology of glucotoxicity.
> > > > >
> > > > Sorry but elevated glucose level causes more secretion of insulin?
> > >
> > > It does until the beta cells become glucotoxic.
> > >
> > Is there any logic behind beta cells damage due to glucotoxicity?
>
> No.
>
Whether lipotoxicity is also directly responsible for beta cells
damage? If yes, in what way it damages?

Can it be possible that direct damages or most damages by glucotoxicity
happens alongwith undelying lipotoxicity?

> > Logically, body mechanism should protect and regenrate more beta cells
> > on gulucotoxicity?
>
> Such is the penalty for overeating.
>
> > Once damaged, whether beta cells don't regenerate?
>
> They can recover.
>
How then diabetic people can get lesser insulin or no insulin
secretion?

Are these permanently damaged after certain stage and by autoimmunity?
 
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