Re: Culprit to Insulin resistance?



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Topic: Religions > Atheism
User: "Andrew B. Chung, MD/PhD"
Date: 19 Nov 2006 05:03:42 AM
Object: Re: Culprit to Insulin resistance?
Kumar wrote:

Hello,

One symptom of hypoglycemia is "hunger" long with other symtoms as
indicated on;
http://www.nlm.nih.gov/medlineplus/ency/article/000386.htm

This is untrue.
Here is evidence:
http://HeartMDPhD.com/HolySpirit/overweight.asp

It means that abnormal insulin's exposure can create hunger to save us
from hypoglycemia.

Simply check you blood glucose when you are hungry and you will see
that hypoglycemia is not the cause.

As such there can be abnormal hunder and overeating
due to abnormal exposure of insulin.

It is clear that you remain brainwashed to hold on to the false belief
that "hunger is bad (abnormal)."
You will have to overcome this brainwashing if you wish to eat less to
lose the visceral adipose tissue (VAT) thereby possible curing your
insulin resistance which is the root source of your type-2 diabetes.

Abnormal insulin exposure can also
be possible due to abnormal eating habits.

Untrue.

It can be thoght that body
mechanism may reduce insulin senstiveness in case of its abnormal
exposure to target cells. Abnormal and continual insulin may cause more
energy storage and lesser breakdown of these. Persisting hyperglycemia
may be thought logically, as an compensation to resisted breakdown of
energy stores by continual insulin's exposure supported by insulin
resistance.

Such thoughts are delusional arising from the false belief that "hunger
is bad."

As such, can we evaluate and consider abnormal, more and continual
insulin's exposure to target cells (natural or added by medication
program) either due to predisposed or aquired reasons be a main culprit
to getting insulin resistance and diabetes2?

No.

We can also try understanding this aspect by understanding different
type of symptoms & no IR in case of IDDM and type1 esp. when insulin
exposure is normal or not more.

Best wishes.

If you understand and take to heart the following true story, you would
no longer hold the false belief that "hunger is bad" which is keeping
you from eating less to lose the VAT that is causing your type-2
diabetes.
Most assuredly, without doubt, I know hunger is good:
http://MabletonGA.OurLittle.net/DreadNought
May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.
Prayerfully in Christ's amazing love,
Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit
As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love
.

User: "Kumar"

Title: Re: Culprit to Insulin resistance? 19 Nov 2006 06:18:25 AM
Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

Hello,

One symptom of hypoglycemia is "hunger" along with other symtoms as
indicated on;
http://www.nlm.nih.gov/medlineplus/ency/article/000386.htm


This is untrue.

Here is evidence:

http://HeartMDPhD.com/HolySpirit/overweight.asp

It means that abnormal insulin's exposure can create hunger to save us
from hypoglycemia.


Simply check you blood glucose when you are hungry and you will see
that hypoglycemia is not the cause.

Hypoglycemia may always cause hunger but greed of food may also cause
cravings. Abnormal insulin secretion or added than normal insulin may
cause excessive hunger or craving. Hunger and overeating eating in such
cases may match with more insulin.
Can we compare total insulin's exposure and food intake in diabetics2
with healthy people?
Can total food intake by diabetic2 be matched with normal insulin
required for that food to a healthy person? Means, more insulin equal
to more food taken by diabetic2.
Whether such hunger and craving as in diabetic2 with IR, is also
saimilar in IDDM or type1?

As such there can be abnormal hunger and overeating
due to abnormal exposure of insulin.


It is clear that you remain brainwashed to hold on to the false belief
that "hunger is bad (abnormal)."

People with hyperglycemia also get hunger and cravings. Whether such
hunger is bad or good?

You will have to overcome this brainwashing if you wish to eat less to
lose the visceral adipose tissue (VAT) thereby possible curing your
insulin resistance which is the root source of your type-2 diabetes.

VATmay interpretIR case. Losing VAT by avoiding overeating can also
cause lesser insulin secretion?

Abnormal insulin exposure can also
be possible due to abnormal eating habits.


Untrue.

In people with insulin resistance and pre-diabetics with overeating,
can more insulin secretion be there or not?

It can be thoght that body
mechanism may reduce insulin senstiveness in case of its abnormal
exposure to target cells. Abnormal and continual insulin may cause more
energy storage and lesser breakdown of these. Persisting hyperglycemia
may be thought logically, as an compensation to resisted breakdown of
energy stores by continual insulin's exposure supported by insulin
resistance.


Such thoughts are delusional arising from the false belief that "hunger
is bad."

Abnormal Hunger occurs in IR cases even thought hyperglycemia is
persisting?

As such, can we evaluate and consider abnormal, more and continual
insulin's exposure to target cells (natural or added by medication
program) either due to predisposed or aquired reasons be a main culprit
to getting insulin resistance and diabetes2?


No.

We may have to match total insulin exposed with total food intake to
evaluate it.

We can also try understanding this aspect by understanding different
type of symptoms & no IR in case of IDDM and type1 esp. when insulin
exposure is normal or not more.

Best wishes.


If you understand and take to heart the following true story, you would
no longer hold the false belief that "hunger is bad" which is keeping
you from eating less to lose the VAT that is causing your type-2
diabetes.

Most assuredly, without doubt, I know hunger is good:

What is persistent hunger or craving, eventhough persisting
hyperglycemia and obesity is persisting?

http://MabletonGA.OurLittle.net/DreadNought

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.

Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love

.
User: "Andrew B. Chung, MD/PhD"

Title: Re: Culprit to Insulin resistance? 19 Nov 2006 07:20:14 AM
Kumar wrote:

Andrew, in the Holy Spirit, boldly wrote:

Kumar wrote:

Hello,

One symptom of hypoglycemia is "hunger" along with other symtoms as
indicated on;
http://www.nlm.nih.gov/medlineplus/ency/article/000386.htm


This is untrue.

Here is evidence:

http://HeartMDPhD.com/HolySpirit/overweight.asp

It means that abnormal insulin's exposure can create hunger to save us
from hypoglycemia.


Simply check you blood glucose when you are hungry and you will see
that hypoglycemia is not the cause.

Hypoglycemia may always cause hunger

Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.
<rest of text read and understood as evidence of continued brainwashed
state and then snipped>


If you understand and take to heart the following true story, you would
no longer hold the false belief that "hunger is bad" which is keeping
you from eating less to lose the VAT that is causing your type-2
diabetes.

Most assuredly, without doubt, I know hunger is good:


What is persistent hunger or craving, eventhough persisting
hyperglycemia and obesity is persisting?

Healthy and good.

http://MabletonGA.OurLittle.net/DreadNought

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.

Prayerfully in Christ's amazing love,
Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit
As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love
.
User: "Kumar"

Title: Re: Culprit to Insulin resistance? 19 Nov 2006 10:49:52 AM
Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

Andrew, in the Holy Spirit, boldly wrote:

Kumar wrote:

Hello,

One symptom of hypoglycemia is "hunger" along with other symtoms as
indicated on;
http://www.nlm.nih.gov/medlineplus/ency/article/000386.htm


This is untrue.

Here is evidence:

http://HeartMDPhD.com/HolySpirit/overweight.asp

It means that abnormal insulin's exposure can create hunger to save us
from hypoglycemia.


Simply check you blood glucose when you are hungry and you will see
that hypoglycemia is not the cause.


Hypoglycemia may always cause hunger


Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.

<rest of text read and understood as evidence of continued brainwashed
state and then snipped>


If you understand and take to heart the following true story, you would
no longer hold the false belief that "hunger is bad" which is keeping
you from eating less to lose the VAT that is causing your type-2
diabetes.

Most assuredly, without doubt, I know hunger is good:


What is persistent hunger or craving, eventhough persisting
hyperglycemia and obesity is persisting?


Healthy and good.

As such, should anyone go on eating till hunger and craving is there
inspite of persisting hyperglycemia and obesity?

http://MabletonGA.OurLittle.net/DreadNought

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.


Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love

.
User: "Kumar"

Title: Re: Culprit to Insulin resistance? 19 Nov 2006 12:17:57 PM
Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.

Following are important snips;
"..Two other factors significantly affect glucose measurement. The
disparity between venous and whole blood concentrations is greater when
the *hematocrit is high, as in newborns.
...Diabetic hypoglycemia represents a special case with respect to the
relationship of measured glucose and hypoglycemic symptoms for several
reasons. Although home glucose meter readings are sometimes misleading,
the probability that a low reading accompanied by symptoms represents
real hypoglycemia is higher in a person who takes insulin. Second, the
hypoglycemia has a greater chance of progressing to more serious
impairment if not treated, compared to most other forms of hypoglycemia
that occur in adults. **Third, because glucose levels are above normal
most of the time in people with diabetes, hypoglycemic symptoms may
occur at higher thresholds than in people who are normoglycemic most of
the time. For all of these reasons, people with diabetes usually use
higher meter glucose thresholds to determine hypoglycemia.**
...Signs and symptoms of hypoglycemia
Hypoglycemic symptoms and manifestations can be divided into those
produced by the counterregulatory hormones (adrenaline and glucagon)
triggered by the falling glucose, and the neuroglycopenic effects
produced by the reduced brain sugar.
[edit] Adrenergic Manifestations
Shakiness, anxiety, nervousness, tremor
Palpitations, tachycardia
Sweating, feeling of warmth
Pallor, coldness, clamminess
Dilated pupils
[edit] Glucagon Manifestations
*Hunger*, borborygmus
Nausea, vomiting, abdominal discomfort
Neuroglycopenic Manifestations..
http://en.wikipedia.org/wiki/Hypoglycemia "
------
"Common Symptoms of Diabetic Hyperglycemia
If you have diabetes mellitus, the presence of these symptoms can
indicate that blood sugar levels are too high:
Polyphagia (frequent hunger, especially pronounced hunger)
Polydipsia (frequent thirst, especially excessive thirst)
Polyuria (frequent urination, especially excessive urination)
But caution: Frequent hunger without the other two symptoms (which
invariably occur together, absent renal complications, bladder
infections, etc.), can also indicate that blood sugar levels are too
low. This commonly occurs when people who have type 2 diabetes mellitus
take too much oral hypoglycemic medication for the amount of food they
eat. The resulting drop in blood sugar level to below the normal range
prompts a hunger response. This hunger is not usually as pronounced as
in type 1 diabetes mellitus (especially the juvenile onset form).
http://en.wikipedia.org/wiki/Hyperglycemia "
----------
Adjustment of efficiency of transfer of glucose from blood across the
blood-brain barrier into the central nervous system represents a third
form of compensation which occurs more gradually. Levels of glucose
within the central nervous system are normally lower than the blood,
regulated by an incompletely understood transfer process. Chronic
hypoglycemia or hyperglycemia seems to result in an increase or
decrease in efficiency of transfer to maintain CNS levels of glucose
within an optimal range.
Neuroglycopenia without hypoglycemia
A rare metabolic disease of the blood-brain glucose transport system
has been described in which severe neuroglycopenic effects occurred
despite normal blood glucose levels. Low levels of glucose were
discovered in the cerebrospinal fluid (CSF), a condition referred to as
hypoglycorrhacia.
Perhaps a much more common example of the same phenomenon occurs in the
people with poorly controlled type 1 diabetes who develop symptoms of
hypoglycemia at levels of blood glucose which are normal for most
people.
http://en.wikipedia.org/wiki/Neuroglycopenia "
Can above may be the reasons for excessive hunger and to to maintain
hyperglycemia in chronic diabetics?
.
User: "Andrew B. Chung, MD/PhD"

Title: Re: Culprit to Insulin resistance? 20 Nov 2006 02:01:13 AM
Kumar wrote:

Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.



Following are important snips;

"..Two other factors significantly affect glucose measurement. The
disparity between venous and whole blood concentrations is greater when
the *hematocrit is high, as in newborns.

..Diabetic hypoglycemia represents a special case with respect to the
relationship of measured glucose and hypoglycemic symptoms for several
reasons. Although home glucose meter readings are sometimes misleading,
the probability that a low reading accompanied by symptoms represents
real hypoglycemia is higher in a person who takes insulin. Second, the
hypoglycemia has a greater chance of progressing to more serious
impairment if not treated, compared to most other forms of hypoglycemia
that occur in adults. **Third, because glucose levels are above normal
most of the time in people with diabetes, hypoglycemic symptoms may
occur at higher thresholds than in people who are normoglycemic most of
the time. For all of these reasons, people with diabetes usually use
higher meter glucose thresholds to determine hypoglycemia.**
..Signs and symptoms of hypoglycemia
Hypoglycemic symptoms and manifestations can be divided into those
produced by the counterregulatory hormones (adrenaline and glucagon)
triggered by the falling glucose, and the neuroglycopenic effects
produced by the reduced brain sugar.

[edit] Adrenergic Manifestations
Shakiness, anxiety, nervousness, tremor
Palpitations, tachycardia
Sweating, feeling of warmth
Pallor, coldness, clamminess
Dilated pupils

[edit] Glucagon Manifestations
*Hunger*, borborygmus
Nausea, vomiting, abdominal discomfort
Neuroglycopenic Manifestations..
http://en.wikipedia.org/wiki/Hypoglycemia "
------

"Common Symptoms of Diabetic Hyperglycemia
If you have diabetes mellitus, the presence of these symptoms can
indicate that blood sugar levels are too high:

Polyphagia (frequent hunger, especially pronounced hunger)
Polydipsia (frequent thirst, especially excessive thirst)
Polyuria (frequent urination, especially excessive urination)
But caution: Frequent hunger without the other two symptoms (which
invariably occur together, absent renal complications, bladder
infections, etc.), can also indicate that blood sugar levels are too
low. This commonly occurs when people who have type 2 diabetes mellitus
take too much oral hypoglycemic medication for the amount of food they
eat. The resulting drop in blood sugar level to below the normal range
prompts a hunger response. This hunger is not usually as pronounced as
in type 1 diabetes mellitus (especially the juvenile onset form).
http://en.wikipedia.org/wiki/Hyperglycemia "
----------

Adjustment of efficiency of transfer of glucose from blood across the
blood-brain barrier into the central nervous system represents a third
form of compensation which occurs more gradually. Levels of glucose
within the central nervous system are normally lower than the blood,
regulated by an incompletely understood transfer process. Chronic
hypoglycemia or hyperglycemia seems to result in an increase or
decrease in efficiency of transfer to maintain CNS levels of glucose
within an optimal range.
Neuroglycopenia without hypoglycemia
A rare metabolic disease of the blood-brain glucose transport system
has been described in which severe neuroglycopenic effects occurred
despite normal blood glucose levels. Low levels of glucose were
discovered in the cerebrospinal fluid (CSF), a condition referred to as
hypoglycorrhacia.

Perhaps a much more common example of the same phenomenon occurs in the
people with poorly controlled type 1 diabetes who develop symptoms of
hypoglycemia at levels of blood glucose which are normal for most
people.
http://en.wikipedia.org/wiki/Neuroglycopenia "

Can above may be the reasons for excessive hunger and to to maintain
hyperglycemia in chronic diabetics?

Not clinically seen.
Bottomline:
Hunger is good.
Understanding with your heart the following two articles will help you
overcome your current false belief that "hunger is bad."
http://HeartMDPhD.com/HolySpirit/overweight.asp
http://MabletonGA.OurLittle.net/DreadNought
May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.
Prayerfully in Christ's amazing love,
Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit
As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love
.
User: "Kumar"

Title: Re: Culprit to Insulin resistance? 20 Nov 2006 02:33:03 AM
Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.



Following are important snips;

"..Two other factors significantly affect glucose measurement. The
disparity between venous and whole blood concentrations is greater when
the *hematocrit is high, as in newborns.

..Diabetic hypoglycemia represents a special case with respect to the
relationship of measured glucose and hypoglycemic symptoms for several
reasons. Although home glucose meter readings are sometimes misleading,
the probability that a low reading accompanied by symptoms represents
real hypoglycemia is higher in a person who takes insulin. Second, the
hypoglycemia has a greater chance of progressing to more serious
impairment if not treated, compared to most other forms of hypoglycemia
that occur in adults. **Third, because glucose levels are above normal
most of the time in people with diabetes, hypoglycemic symptoms may
occur at higher thresholds than in people who are normoglycemic most of
the time. For all of these reasons, people with diabetes usually use
higher meter glucose thresholds to determine hypoglycemia.**
..Signs and symptoms of hypoglycemia
Hypoglycemic symptoms and manifestations can be divided into those
produced by the counterregulatory hormones (adrenaline and glucagon)
triggered by the falling glucose, and the neuroglycopenic effects
produced by the reduced brain sugar.

[edit] Adrenergic Manifestations
Shakiness, anxiety, nervousness, tremor
Palpitations, tachycardia
Sweating, feeling of warmth
Pallor, coldness, clamminess
Dilated pupils

[edit] Glucagon Manifestations
*Hunger*, borborygmus
Nausea, vomiting, abdominal discomfort
Neuroglycopenic Manifestations..
http://en.wikipedia.org/wiki/Hypoglycemia "
------

"Common Symptoms of Diabetic Hyperglycemia
If you have diabetes mellitus, the presence of these symptoms can
indicate that blood sugar levels are too high:

Polyphagia (frequent hunger, especially pronounced hunger)
Polydipsia (frequent thirst, especially excessive thirst)
Polyuria (frequent urination, especially excessive urination)
But caution: Frequent hunger without the other two symptoms (which
invariably occur together, absent renal complications, bladder
infections, etc.), can also indicate that blood sugar levels are too
low. This commonly occurs when people who have type 2 diabetes mellitus
take too much oral hypoglycemic medication for the amount of food they
eat. The resulting drop in blood sugar level to below the normal range
prompts a hunger response. This hunger is not usually as pronounced as
in type 1 diabetes mellitus (especially the juvenile onset form).
http://en.wikipedia.org/wiki/Hyperglycemia "
----------

Adjustment of efficiency of transfer of glucose from blood across the
blood-brain barrier into the central nervous system represents a third
form of compensation which occurs more gradually. Levels of glucose
within the central nervous system are normally lower than the blood,
regulated by an incompletely understood transfer process. Chronic
hypoglycemia or hyperglycemia seems to result in an increase or
decrease in efficiency of transfer to maintain CNS levels of glucose
within an optimal range.
Neuroglycopenia without hypoglycemia
A rare metabolic disease of the blood-brain glucose transport system
has been described in which severe neuroglycopenic effects occurred
despite normal blood glucose levels. Low levels of glucose were
discovered in the cerebrospinal fluid (CSF), a condition referred to as
hypoglycorrhacia.

Perhaps a much more common example of the same phenomenon occurs in the
people with poorly controlled type 1 diabetes who develop symptoms of
hypoglycemia at levels of blood glucose which are normal for most
people.
http://en.wikipedia.org/wiki/Neuroglycopenia "

Can above may be the reasons for excessive hunger and to to maintain
hyperglycemia in chronic diabetics?


Not clinically seen.

Bottomline:

Hunger is good.

Understanding with your heart the following two articles will help you
overcome your current false belief that "hunger is bad."

http://HeartMDPhD.com/HolySpirit/overweight.asp

http://MabletonGA.OurLittle.net/DreadNought

Read; thanks. But I have some thoughts...i.e. resisting energy store
breakdown by continual insulin's exposure & so body system may maintain
alternative compensatory hyperglycemia for immediate need OR due to
either some impairmrent in glucose supply to briain, some tolerance to
glucose or decreased movement of insulin or glucose to extravascular
tissues either due to vasoconstriction/decreased blood flow or due to
cells swellings & vascular intimal inflammation(it may resist insulin's
filteration, it being bigger molecule)?

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.

Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love

.
User: "Andrew B. Chung, MD/PhD"

Title: Re: Culprit to Insulin resistance? 20 Nov 2006 03:09:49 AM
Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.



Following are important snips;

"..Two other factors significantly affect glucose measurement. The
disparity between venous and whole blood concentrations is greater when
the *hematocrit is high, as in newborns.

..Diabetic hypoglycemia represents a special case with respect to the
relationship of measured glucose and hypoglycemic symptoms for several
reasons. Although home glucose meter readings are sometimes misleading,
the probability that a low reading accompanied by symptoms represents
real hypoglycemia is higher in a person who takes insulin. Second, the
hypoglycemia has a greater chance of progressing to more serious
impairment if not treated, compared to most other forms of hypoglycemia
that occur in adults. **Third, because glucose levels are above normal
most of the time in people with diabetes, hypoglycemic symptoms may
occur at higher thresholds than in people who are normoglycemic most of
the time. For all of these reasons, people with diabetes usually use
higher meter glucose thresholds to determine hypoglycemia.**
..Signs and symptoms of hypoglycemia
Hypoglycemic symptoms and manifestations can be divided into those
produced by the counterregulatory hormones (adrenaline and glucagon)
triggered by the falling glucose, and the neuroglycopenic effects
produced by the reduced brain sugar.

[edit] Adrenergic Manifestations
Shakiness, anxiety, nervousness, tremor
Palpitations, tachycardia
Sweating, feeling of warmth
Pallor, coldness, clamminess
Dilated pupils

[edit] Glucagon Manifestations
*Hunger*, borborygmus
Nausea, vomiting, abdominal discomfort
Neuroglycopenic Manifestations..
http://en.wikipedia.org/wiki/Hypoglycemia "
------

"Common Symptoms of Diabetic Hyperglycemia
If you have diabetes mellitus, the presence of these symptoms can
indicate that blood sugar levels are too high:

Polyphagia (frequent hunger, especially pronounced hunger)
Polydipsia (frequent thirst, especially excessive thirst)
Polyuria (frequent urination, especially excessive urination)
But caution: Frequent hunger without the other two symptoms (which
invariably occur together, absent renal complications, bladder
infections, etc.), can also indicate that blood sugar levels are too
low. This commonly occurs when people who have type 2 diabetes mellitus
take too much oral hypoglycemic medication for the amount of food they
eat. The resulting drop in blood sugar level to below the normal range
prompts a hunger response. This hunger is not usually as pronounced as
in type 1 diabetes mellitus (especially the juvenile onset form).
http://en.wikipedia.org/wiki/Hyperglycemia "
----------

Adjustment of efficiency of transfer of glucose from blood across the
blood-brain barrier into the central nervous system represents a third
form of compensation which occurs more gradually. Levels of glucose
within the central nervous system are normally lower than the blood,
regulated by an incompletely understood transfer process. Chronic
hypoglycemia or hyperglycemia seems to result in an increase or
decrease in efficiency of transfer to maintain CNS levels of glucose
within an optimal range.
Neuroglycopenia without hypoglycemia
A rare metabolic disease of the blood-brain glucose transport system
has been described in which severe neuroglycopenic effects occurred
despite normal blood glucose levels. Low levels of glucose were
discovered in the cerebrospinal fluid (CSF), a condition referred to as
hypoglycorrhacia.

Perhaps a much more common example of the same phenomenon occurs in the
people with poorly controlled type 1 diabetes who develop symptoms of
hypoglycemia at levels of blood glucose which are normal for most
people.
http://en.wikipedia.org/wiki/Neuroglycopenia "

Can above may be the reasons for excessive hunger and to to maintain
hyperglycemia in chronic diabetics?


Not clinically seen.

Bottomline:

Hunger is good.

Understanding with your heart the following two articles will help you
overcome your current false belief that "hunger is bad."

http://HeartMDPhD.com/HolySpirit/overweight.asp

http://MabletonGA.OurLittle.net/DreadNought


Read; thanks.

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

But I have some thoughts...i.e. resisting energy store
breakdown by continual insulin's exposure & so body system may maintain
alternative compensatory hyperglycemia for immediate need OR due to
either some impairmrent in glucose supply to briain, some tolerance to
glucose or decreased movement of insulin or glucose to extravascular
tissues either due to vasoconstriction/decreased blood flow or due to
cells swellings & vascular intimal inflammation(it may resist insulin's
filteration, it being bigger molecule)?

Not clinically seen.
Most assuredly, without doubt, I know hunger to be good.
May you also someday know this in your heart.

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.

Prayerfully in Christ's amazing love,
Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit
As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love
.




User: "Andrew B. Chung, MD/PhD"

Title: Re: Culprit to Insulin resistance? 20 Nov 2006 02:01:18 AM
Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

Andrew, in the Holy Spirit, boldly wrote:

Kumar wrote:

Hello,

One symptom of hypoglycemia is "hunger" along with other symtoms as
indicated on;
http://www.nlm.nih.gov/medlineplus/ency/article/000386.htm


This is untrue.

Here is evidence:

http://HeartMDPhD.com/HolySpirit/overweight.asp

It means that abnormal insulin's exposure can create hunger to save us
from hypoglycemia.


Simply check you blood glucose when you are hungry and you will see
that hypoglycemia is not the cause.


Hypoglycemia may always cause hunger


Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.

<rest of text read and understood as evidence of continued brainwashed
state and then snipped>


If you understand and take to heart the following true story, you would
no longer hold the false belief that "hunger is bad" which is keeping
you from eating less to lose the VAT that is causing your type-2
diabetes.

Most assuredly, without doubt, I know hunger is good:

http://MabletonGA.OurLittle.net/DreadNought


What is persistent hunger or craving, eventhough persisting
hyperglycemia and obesity is persisting?


Healthy and good.


As such, should anyone go on eating till hunger and craving is there
inspite of persisting hyperglycemia and obesity?

One should stop eating before one is full:
http://HeartMDPhD.com/HolySpirit/overweight.asp

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.

Prayerfully in Christ's amazing love,
Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit
As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love
.
User: "Kumar"

Title: Re: Culprit to Insulin resistance? 20 Nov 2006 02:50:08 AM
Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

Andrew, in the Holy Spirit, boldly wrote:

Kumar wrote:

Hello,

One symptom of hypoglycemia is "hunger" along with other symtoms as
indicated on;
http://www.nlm.nih.gov/medlineplus/ency/article/000386.htm


This is untrue.

Here is evidence:

http://HeartMDPhD.com/HolySpirit/overweight.asp

It means that abnormal insulin's exposure can create hunger to save us
from hypoglycemia.


Simply check you blood glucose when you are hungry and you will see
that hypoglycemia is not the cause.


Hypoglycemia may always cause hunger


Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.

<rest of text read and understood as evidence of continued brainwashed
state and then snipped>


If you understand and take to heart the following true story, you would
no longer hold the false belief that "hunger is bad" which is keeping
you from eating less to lose the VAT that is causing your type-2
diabetes.

Most assuredly, without doubt, I know hunger is good:

http://MabletonGA.OurLittle.net/DreadNought


What is persistent hunger or craving, eventhough persisting
hyperglycemia and obesity is persisting?


Healthy and good.


As such, should anyone go on eating till hunger and craving is there
inspite of persisting hyperglycemia and obesity?


One should stop eating before one is full:

http://HeartMDPhD.com/HolySpirit/overweight.asp

Basically, why one feel hunger and craving if he already has persisting
hyperglycemia and obesity?
Whether intimal's cells swelling/inflammation can resist insulin's
movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?
Can foods with low Glycemic index or Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?
As such whether nuts and other food with low GI/GL are beneficial in
diabetes?

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.


Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love

.
User: "Andrew B. Chung, MD/PhD"

Title: Re: Culprit to Insulin resistance? 20 Nov 2006 03:09:39 AM
Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

Andrew, in the Holy Spirit, boldly wrote:

Kumar wrote:

Hello,

One symptom of hypoglycemia is "hunger" along with other symtoms as
indicated on;
http://www.nlm.nih.gov/medlineplus/ency/article/000386.htm


This is untrue.

Here is evidence:

http://HeartMDPhD.com/HolySpirit/overweight.asp

It means that abnormal insulin's exposure can create hunger to save us
from hypoglycemia.


Simply check you blood glucose when you are hungry and you will see
that hypoglycemia is not the cause.


Hypoglycemia may always cause hunger


Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.

<rest of text read and understood as evidence of continued brainwashed
state and then snipped>


If you understand and take to heart the following true story, you would
no longer hold the false belief that "hunger is bad" which is keeping
you from eating less to lose the VAT that is causing your type-2
diabetes.

Most assuredly, without doubt, I know hunger is good:

http://MabletonGA.OurLittle.net/DreadNought


What is persistent hunger or craving, eventhough persisting
hyperglycemia and obesity is persisting?


Healthy and good.


As such, should anyone go on eating till hunger and craving is there
inspite of persisting hyperglycemia and obesity?


One should stop eating before one is full:

http://HeartMDPhD.com/HolySpirit/overweight.asp


Basically, why one feel hunger and craving if he already has persisting
hyperglycemia and obesity?

Because one is otherwise healthy.

Whether intimal's cells swelling/inflammation can resist insulin's
movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?

Not clinically seen.

Can foods with low Glycemic index or Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?

Wiser to simply eat less down to the optimal amount:
http://HeartMDPhD.com/HolySpirit/overweight.asp

As such whether nuts and other food with low GI/GL are beneficial in
diabetes?

Wiser to simply befriend the hunger that will grow much bigger with
eating less down to the optimal amount:
http://MabletonGA.OurLittle.net/DreadNought
May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.
Prayerfully in Christ's amazing love,
Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit
As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love
.
User: "Kumar"

Title: Re: Culprit to Insulin resistance? 20 Nov 2006 04:59:47 AM
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, in the Holy Spirit, boldly wrote:

Kumar wrote:

Hello,

One symptom of hypoglycemia is "hunger" along with other symtoms as
indicated on;
http://www.nlm.nih.gov/medlineplus/ency/article/000386.htm


This is untrue.

Here is evidence:

http://HeartMDPhD.com/HolySpirit/overweight.asp

It means that abnormal insulin's exposure can create hunger to save us
from hypoglycemia.


Simply check you blood glucose when you are hungry and you will see
that hypoglycemia is not the cause.


Hypoglycemia may always cause hunger


Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.

<rest of text read and understood as evidence of continued brainwashed
state and then snipped>


If you understand and take to heart the following true story, you would
no longer hold the false belief that "hunger is bad" which is keeping
you from eating less to lose the VAT that is causing your type-2
diabetes.

Most assuredly, without doubt, I know hunger is good:

http://MabletonGA.OurLittle.net/DreadNought


What is persistent hunger or craving, eventhough persisting
hyperglycemia and obesity is persisting?


Healthy and good.


As such, should anyone go on eating till hunger and craving is there
inspite of persisting hyperglycemia and obesity?


One should stop eating before one is full:

http://HeartMDPhD.com/HolySpirit/overweight.asp


Basically, why one feel hunger and craving if he already has persisting
hyperglycemia and obesity?


Because one is otherwise healthy.

Whether intimal's cells swelling/inflammation can resist insulin's
movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?


Not clinically seen.

Pls tell me again about decreased supply due to intimal inflammation
causing arthritis?

Can foods with low Glycemic index or Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


Wiser to simply eat less down to the optimal amount:

http://HeartMDPhD.com/HolySpirit/overweight.asp

Yes, *optimal food intake* should be perfect practice. But I want to
know it for some other possibility?Can foods with low Glycemic index or
Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?

As such whether nuts and other food with low GI/GL are beneficial in
diabetes?

How low GI/GL foods can cause insulin secretion? Can it be continual?

Wiser to simply befriend the hunger that will grow much bigger with
eating less down to the optimal amount:

http://MabletonGA.OurLittle.net/DreadNought

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.

Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love

.
User: "Andrew B. Chung, MD/PhD"

Title: Re: Culprit to Insulin resistance? 20 Nov 2006 05:22:27 AM
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, in the Holy Spirit, boldly wrote:

Kumar wrote:

Hello,

One symptom of hypoglycemia is "hunger" along with other symtoms as
indicated on;
http://www.nlm.nih.gov/medlineplus/ency/article/000386.htm


This is untrue.

Here is evidence:

http://HeartMDPhD.com/HolySpirit/overweight.asp

It means that abnormal insulin's exposure can create hunger to save us
from hypoglycemia.


Simply check you blood glucose when you are hungry and you will see
that hypoglycemia is not the cause.


Hypoglycemia may always cause hunger


Actually, the adrenaline that is always released in response to
hypoglycemia ensures that people are not hungry but trembly, shaky, and
diaphoretic instead.

<rest of text read and understood as evidence of continued brainwashed
state and then snipped>


If you understand and take to heart the following true story, you would
no longer hold the false belief that "hunger is bad" which is keeping
you from eating less to lose the VAT that is causing your type-2
diabetes.

Most assuredly, without doubt, I know hunger is good:

http://MabletonGA.OurLittle.net/DreadNought


What is persistent hunger or craving, eventhough persisting
hyperglycemia and obesity is persisting?


Healthy and good.


As such, should anyone go on eating till hunger and craving is there
inspite of persisting hyperglycemia and obesity?


One should stop eating before one is full:

http://HeartMDPhD.com/HolySpirit/overweight.asp


Basically, why one feel hunger and craving if he already has persisting
hyperglycemia and obesity?


Because one is otherwise healthy.

Whether intimal's cells swelling/inflammation can resist insulin's
movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?


Not clinically seen.

Pls tell me again about decreased supply due to intimal inflammation
causing arthritis?

Osteoarthritis, which is the most common arthritis affecting adults, is
likely caused by microvascular problems arising from microvascular
inflammation driven by VAT.

Can foods with low Glycemic index or Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


Wiser to simply eat less down to the optimal amount:

http://HeartMDPhD.com/HolySpirit/overweight.asp


Yes, *optimal food intake* should be perfect practice. But I want to
know it for some other possibility?Can foods with low Glycemic index or
Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?

It seems wisdom escapes you at the moment.

As such whether nuts and other food with low GI/GL are beneficial in
diabetes?

How low GI/GL foods can cause insulin secretion? Can it be continual?

It still seems that wisdom escapes you.

Wiser to simply befriend the hunger that will grow much bigger with
eating less down to the optimal amount:

http://MabletonGA.OurLittle.net/DreadNought

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.

Prayerfully in Christ's amazing love,
Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit
As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love
.
User: "kumar"

Title: Re: Culprit to Insulin resistance? 20 Nov 2006 08:54:05 AM
Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

snip> > > > Whether intimal's cells swelling/inflammation can resist
insulin's

movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?


Not clinically seen.


Pls tell me again about decreased supply due to intimal inflammation
causing arthritis?


Osteoarthritis, which is the most common arthritis affecting adults, is
likely caused by microvascular problems arising from microvascular
inflammation driven by VAT.

Whether such microvascular problem/inflammation is atherosclerosis or
by cell's welling due to hyotonicity of blood in comparsn to
hypertonicity of vescular wall cells? Can endothelial cells in intima,
smooth muscle cells and elastic tissue in media and connective tissues
in adventitia take water and swell/brust in hypotonic environment?

Can foods with low Glycemic index or Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


Wiser to simply eat less down to the optimal amount:

http://HeartMDPhD.com/HolySpirit/overweight.asp


Yes, *optimal food intake* should be perfect practice. But I want to
know it for some other possibility?Can foods with low Glycemic index or
Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


It seems wisdom escapes you at the moment.

As such whether nuts and other food with low GI/GL are beneficial in
diabetes?


How low GI/GL foods can cause insulin secretion? Can it be continual?


It still seems that wisdom escapes you.

"Carbohydrates that break down rapidly during digestion have the
highest glycemic indices. Such carbohydrates require less energy to be
converted into glucose, which results in faster digestion and a quicker
increase of blood glucose. Carbohydrates that break down slowly,
releasing glucose gradually into the blood stream, have a low glycemic
index. A lower glycemic index suggests slower rates of digestion and
absorption of the sugars and starches in the foods and may also
indicate greater extraction from the liver and periphery of the
products of carbohydrate digestion. Additionally, a lower glycemic
response equates to a lower insulin demand, better long-term blood
glucose control and a reduction in blood lipids.
http://en.wikipedia.org/wiki/Glycemic_index "
I meant above.
As such, will food with low GI can cause lower but prolonged/continual
insulin's secretion/demand?

Wiser to simply befriend the hunger that will grow much bigger with
eating less down to the optimal amount:

http://MabletonGA.OurLittle.net/DreadNought

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.


Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love

.
User: "Andrew B. Chung, MD/PhD"

Title: Re: Culprit to Insulin resistance? 21 Nov 2006 04:00:17 AM
kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

snip> > > > Whether intimal's cells swelling/inflammation can resist
insulin's

movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?


Not clinically seen.


Pls tell me again about decreased supply due to intimal inflammation
causing arthritis?


Osteoarthritis, which is the most common arthritis affecting adults, is
likely caused by microvascular problems arising from microvascular
inflammation driven by VAT.

Whether such microvascular problem/inflammation is atherosclerosis or
by cell's welling due to hyotonicity of blood in comparsn to
hypertonicity of vescular wall cells?

Neither.
It is obliteration of the microvasculature.

Can endothelial cells in intima,
smooth muscle cells and elastic tissue in media and connective tissues
in adventitia take water and swell/brust in hypotonic environment?

The latter is not clinically seen.

Can foods with low Glycemic index or Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


Wiser to simply eat less down to the optimal amount:

http://HeartMDPhD.com/HolySpirit/overweight.asp


Yes, *optimal food intake* should be perfect practice. But I want to
know it for some other possibility?Can foods with low Glycemic index or
Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


It seems wisdom escapes you at the moment.

As such whether nuts and other food with low GI/GL are beneficial in
diabetes?


How low GI/GL foods can cause insulin secretion? Can it be continual?


It still seems that wisdom escapes you.


"Carbohydrates that break down rapidly during digestion have the
highest glycemic indices. Such carbohydrates require less energy to be
converted into glucose, which results in faster digestion and a quicker
increase of blood glucose. Carbohydrates that break down slowly,
releasing glucose gradually into the blood stream, have a low glycemic
index. A lower glycemic index suggests slower rates of digestion and
absorption of the sugars and starches in the foods and may also
indicate greater extraction from the liver and periphery of the
products of carbohydrate digestion. Additionally, a lower glycemic
response equates to a lower insulin demand, better long-term blood
glucose control and a reduction in blood lipids.
http://en.wikipedia.org/wiki/Glycemic_index "

I meant above.

Nothing on-line will give you wisdom.
Only GOD can give you wisdom.

As such, will food with low GI can cause lower but prolonged/continual
insulin's secretion/demand?

Not germane to the cause of insulin resistance which is the VAT that
arises from overeating.

Wiser to simply befriend the hunger that will grow much bigger with
eating less down to the optimal amount:

http://MabletonGA.OurLittle.net/DreadNought

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.

Prayerfully in Christ's amazing love,
Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit
As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love
.
User: "Kumar"

Title: Re: Culprit to Insulin resistance? 21 Nov 2006 04:32:10 AM
Andrew B. Chung, MD/PhD wrote:

kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

snip> > > > Whether intimal's cells swelling/inflammation can resist
insulin's

movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?


Not clinically seen.


Pls tell me again about decreased supply due to intimal inflammation
causing arthritis?


Osteoarthritis, which is the most common arthritis affecting adults, is
likely caused by microvascular problems arising from microvascular
inflammation driven by VAT.


Whether such microvascular problem/inflammation is atherosclerosis or
by cell's welling due to hyotonicity of blood in comparsn to
hypertonicity of vescular wall cells?


Neither.

It is obliteration of the microvasculature.

What is it?

Can endothelial cells in intima,
smooth muscle cells and elastic tissue in media and connective tissues
in adventitia take water and swell/brust in hypotonic environment?


The latter is not clinically seen.

In formers?
In short, can there be some defect in mirovessels which may resist or
restrict transcapillary movement of insulin? [ I now started thinking,
if such insulin movement is controlled by changes in glucose oriented
changes in tonicity of blood resulting into change in the size of
cells wall tissues(endoth. cell swelling) restricting transcaillary
movement of bigger molecules as insulin may be one reason to decresed
effect of insulin]?

Can foods with low Glycemic index or Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


Wiser to simply eat less down to the optimal amount:

http://HeartMDPhD.com/HolySpirit/overweight.asp


Yes, *optimal food intake* should be perfect practice. But I want to
know it for some other possibility?Can foods with low Glycemic index or
Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


It seems wisdom escapes you at the moment.

As such whether nuts and other food with low GI/GL are beneficial in
diabetes?


How low GI/GL foods can cause insulin secretion? Can it be continual?


It still seems that wisdom escapes you.


"Carbohydrates that break down rapidly during digestion have the
highest glycemic indices. Such carbohydrates require less energy to be
converted into glucose, which results in faster digestion and a quicker
increase of blood glucose. Carbohydrates that break down slowly,
releasing glucose gradually into the blood stream, have a low glycemic
index. A lower glycemic index suggests slower rates of digestion and
absorption of the sugars and starches in the foods and may also
indicate greater extraction from the liver and periphery of the
products of carbohydrate digestion. Additionally, a lower glycemic
response equates to a lower insulin demand, better long-term blood
glucose control and a reduction in blood lipids.
http://en.wikipedia.org/wiki/Glycemic_index "

I meant above.


Nothing on-line will give you wisdom.

Only GOD can give you wisdom.

As such, will food with low GI can cause lower but prolonged/continual
insulin's secretion/demand?


Not germane to the cause of insulin resistance which is the VAT that
arises from overeating.

Wiser to simply befriend the hunger that will grow much bigger with
eating less down to the optimal amount:

http://MabletonGA.OurLittle.net/DreadNought

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.


Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love

.
User: "Kumar"

Title: Re: Culprit to Insulin resistance? 23 Nov 2006 03:17:58 AM
Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

snip> > > > Whether intimal's cells swelling/inflammation can resist
insulin's

movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?


Not clinically seen.


Pls tell me again about decreased supply due to intimal inflammation
causing arthritis?


Osteoarthritis, which is the most common arthritis affecting adults, is
likely caused by microvascular problems arising from microvascular
inflammation driven by VAT.


Whether such microvascular problem/inflammation is atherosclerosis or
by cell's welling due to hyotonicity of blood in comparsn to
hypertonicity of vescular wall cells?


Neither.

It is obliteration of the microvasculature.


What is it?

Can endothelial cells in intima,
smooth muscle cells and elastic tissue in media and connective tissues
in adventitia take water and swell/brust in hypotonic environment?


The latter is not clinically seen.


In formers?

In short, can there be some defect in mirovessels which may resist or
restrict transcapillary movement of insulin? [ I now started thinking,
if such insulin movement is controlled by changes in glucose oriented
changes in tonicity of blood resulting into change in the size of
cells wall tissues(endoth. cell swelling) restricting transcaillary
movement of bigger molecules as insulin may be one reason to decresed
effect of insulin]?

Can foods with low Glycemic index or Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


Wiser to simply eat less down to the optimal amount:

http://HeartMDPhD.com/HolySpirit/overweight.asp


Yes, *optimal food intake* should be perfect practice. But I want to
know it for some other possibility?Can foods with low Glycemic index or
Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


It seems wisdom escapes you at the moment.

As such whether nuts and other food with low GI/GL are beneficial in
diabetes?


How low GI/GL foods can cause insulin secretion? Can it be continual?


It still seems that wisdom escapes you.


"Carbohydrates that break down rapidly during digestion have the
highest glycemic indices. Such carbohydrates require less energy to be
converted into glucose, which results in faster digestion and a quicker
increase of blood glucose. Carbohydrates that break down slowly,
releasing glucose gradually into the blood stream, have a low glycemic
index. A lower glycemic index suggests slower rates of digestion and
absorption of the sugars and starches in the foods and may also
indicate greater extraction from the liver and periphery of the
products of carbohydrate digestion. Additionally, a lower glycemic
response equates to a lower insulin demand, better long-term blood
glucose control and a reduction in blood lipids.
http://en.wikipedia.org/wiki/Glycemic_index "

I meant above.


Nothing on-line will give you wisdom.

Only GOD can give you wisdom.

As such, will food with low GI can cause lower but prolonged/continual
insulin's secretion/demand?


Not germane to the cause of insulin resistance which is the VAT that
arises from overeating.

Wiser to simply befriend the hunger that will grow much bigger with
eating less down to the optimal amount:

http://MabletonGA.OurLittle.net/DreadNought

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.


Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love

To add;
"..Delayed Transcapillary Transport of Insulin to Muscle Interstitial
Fluid in Obese Subjects:
In summary, the present data show for the first time that obese humans
have a delayed distribution of insulin-to-muscle interstitial fluid as
well as a slower activation of the glucose uptake rate. These data
suggest that a delayed delivery of insulin may contribute to muscle
insulin resistance in obesity.
http://diabetes.diabetesjournals.org/cgi/content/full/51/9/2742 "
As such what factors can be responsible for Delayed Transcapillary
Transport of Insulin to Muscle Interstitial Fluid?
.

User: "Andrew B. Chung, MD/PhD"

Title: Re: Culprit to Insulin resistance? 23 Nov 2006 03:30:12 AM
Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

snip> > > > Whether intimal's cells swelling/inflammation can resist
insulin's

movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?


Not clinically seen.


Pls tell me again about decreased supply due to intimal inflammation
causing arthritis?


Osteoarthritis, which is the most common arthritis affecting adults, is
likely caused by microvascular problems arising from microvascular
inflammation driven by VAT.


Whether such microvascular problem/inflammation is atherosclerosis or
by cell's welling due to hyotonicity of blood in comparsn to
hypertonicity of vescular wall cells?


Neither.

It is obliteration of the microvasculature.


What is it?

Loss of capillaries.

Can endothelial cells in intima,
smooth muscle cells and elastic tissue in media and connective tissues
in adventitia take water and swell/brust in hypotonic environment?


The latter is not clinically seen.


In formers?

You wouldn't be able to swim in lakes and rivers without exploding
otherwise.

In short, can there be some defect in mirovessels which may resist or
restrict transcapillary movement of insulin? [ I now started thinking,
if such insulin movement is controlled by changes in glucose oriented
changes in tonicity of blood resulting into change in the size of
cells wall tissues(endoth. cell swelling) restricting transcaillary
movement of bigger molecules as insulin may be one reason to decresed
effect of insulin]?

Not clinically seen.

Can foods with low Glycemic index or Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


Wiser to simply eat less down to the optimal amount:

http://HeartMDPhD.com/HolySpirit/overweight.asp


Yes, *optimal food intake* should be perfect practice. But I want to
know it for some other possibility?Can foods with low Glycemic index or
Load are absorbed & metabolize
slowly resulting slower but prolonged increase in glucose as opposite
to food with high GI and GL index?


It seems wisdom escapes you at the moment.

As such whether nuts and other food with low GI/GL are beneficial in
diabetes?


How low GI/GL foods can cause insulin secretion? Can it be continual?


It still seems that wisdom escapes you.


"Carbohydrates that break down rapidly during digestion have the
highest glycemic indices. Such carbohydrates require less energy to be
converted into glucose, which results in faster digestion and a quicker
increase of blood glucose. Carbohydrates that break down slowly,
releasing glucose gradually into the blood stream, have a low glycemic
index. A lower glycemic index suggests slower rates of digestion and
absorption of the sugars and starches in the foods and may also
indicate greater extraction from the liver and periphery of the
products of carbohydrate digestion. Additionally, a lower glycemic
response equates to a lower insulin demand, better long-term blood
glucose control and a reduction in blood lipids.
http://en.wikipedia.org/wiki/Glycemic_index "

I meant above.


Nothing on-line will give you wisdom.

Only GOD can give you wisdom.

As such, will food with low GI can cause lower but prolonged/continual
insulin's secretion/demand?


Not germane to the cause of insulin resistance which is the VAT that
arises from overeating.

Wiser to simply befriend the hunger that will grow much bigger with
eating less down to the optimal amount:

http://MabletonGA.OurLittle.net/DreadNought

May GOD continue to heal your heart by curing your diabetes, dear
neighbor Kumar whom I love unconditionally.

Prayerfully in Christ's amazing love,
Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit
As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love
.
User: "Kumar"

Title: Re: Culprit to Insulin resistance? 23 Nov 2006 03:56:04 AM
Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

Andrew B. Chung, MD/PhD wrote:

kumar wrote:

Andrew B. Chung, MD/PhD wrote:

Kumar wrote:

snip> > > > Whether intimal's cells swelling/inflammation can resist
insulin's

movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?


Not clinically seen.


Pls tell me again about decreased supply due to intimal inflammation
causing arthritis?


Osteoarthritis, which is the most common arthritis affecting adults, is
likely caused by microvascular problems arising from microvascular
inflammation driven by VAT.


Whether such microvascular problem/inflammation is atherosclerosis or
by cell's swelling due to hyotonicity of blood in comparisn to
hypertonicity of vescular wall cells?


Neither.

It is obliteration of the microvasculature.


What is it?


Loss of capillaries.

Pls look at following studies[sorry bit long but important];
To add;
"..Delayed Transcapillary Transport of Insulin to Muscle Interstitial
Fluid in Obese Subjects:
In summary, the present data show for the first time that obese humans
have a delayed distribution of insulin-to-muscle interstitial fluid as
well as a slower activation of the glucose uptake rate. These data
suggest that a delayed delivery of insulin may contribute to muscle
insulin resistance in obesity.
http://diabetes.diabetesjournals.org/cgi/content/full/51/9/2742 "
": Diabetes. 2005 Jan;54(1):152-7. Links
Retraction in:
Sjostrand M, Gudbjornsdottir S, Strindberg L, Lonnroth P. Diabetes.
2005 Jul;54(7):2266.
Delayed transcapillary delivery of insulin to muscle interstitial fluid
after oral glucose load in obese subjects.
Sjostrand M, Gudbjornsdottir S, Strindberg L, Lonnroth P.
Lundberg Laboratory for Diabetes Research, Sahlgrenska University
Hospital, S-41345 Goteborg, Sweden.

Obese subjects exhibit a delay in insulin action and delivery of
insulin to muscle interstitial fluid during glucose/insulin infusion.
The aim of the present study was to follow the distribution of insulin
to skeletal muscle after an oral glucose load in obese subjects. We
conducted an oral glucose tolerance test (OGTT) in 10 lean and 10 obese
subjects (BMI 23 +/- 0.6 vs. 33 +/- 1.2 kg/m(2); P < 0.001). Insulin
measurements in muscle interstitial fluid were combined with forearm
arteriovenous catheterization and blood flow measurements. In the obese
group, interstitial insulin was significantly (35-55%) lower than
plasma insulin (P < 0.05) during the 1st h after the OGTT, whereas in
lean subjects, no significant difference was found between interstitial
and plasma insulin levels during the same time period. The permeability
surface area product for glucose, representing capillary recruitment,
increased in the lean group (P < 0.05) but not in the obese group (NS).
Obese subjects had a significantly higher plasma insulin level at
90-120 min after oral glucose (398 +/- 57 vs. 224 +/- 37 pmol/l in
control subjects; P < 0.05). The significant gradient between plasma
insulin and muscle interstitial insulin during the first hour after
OGTT suggests a slow delivery of insulin in obese subjects. The
hindered transcapillary transport of insulin may be attributable to a
defect in insulin-mediated capillary recruitment.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15616023&dopt=Abstract
"
1: Diabetes. 2000 Jul;49(7):1178-85. Links
Muscle glucose uptake is effectively activated by ischemia in type 2
diabetic subjects.
Niklasson M, Holmang A, Sjostrand M, Strindberg L, Lonnroth P.
Department of Heart and Lung Diseases, Sahlgrenska University Hospital,
Goteborg, Sweden.

It has previously been shown that Wortmannin, a phosphatidylinositol
3-kinase inhibitor, inhibits glucose transport activated by insulin but
not by ischemia, suggesting the importance of an activating mechanism
that bypasses the insulin signal. To evaluate the relevance of this
insulin-independent pathway in insulin-resistant subjects, the ability
of ischemia to stimulate glucose uptake was investigated in 9 patients
with type 2 diabetes and in 9 healthy control subjects (fasting glucose
level 9.4 +/- 0.8 vs. 5.1 +/- 0.1 mmol/l, P < 0.001, in type 2 diabetic
patients and control subjects, respectively; fasting insulin level
insulin 8.1 +/- 2.6 vs. 4.5 +/-0.7 mU/l, P < 0.05, respectively)
matched for sex, age, and BMI. Arterial plasma and interstitial
concentrations of glucose and lactate (measured by subcutaneous and
muscle microdialysis) were recorded in the forearm before, during, and
after ischemia induced locally for 20 min. During ischemia, the muscle
interstitial glucose concentration decreased significantly from 7.7 +/-
0.6 to 5.4 +/- 0.4 mmol/l (P < 0.01) and from 4.4 +/- 0.3 to 3.6 +/-
0.3 mmol/l (P < 0.05) in type 2 diabetic patients and control subjects,
respectively. The arterial-interstitial (A-I) glucose concentration
difference was 1.7 +/- 0.6 and 0.7 +/- 0.3 mmol/ at basal, and it
increased significantly to 3.5 +/- 0.7 (P < 0.01) and 1.4 +/-0.3 mmol/l
(P < 0.05) during ischemia in each group, respectively. Interstitial
lactate increased significantly during ischemia from 0.8 +/- 0.1 to 1.1
+/- 0.1 mmol/l (P < 0.05) and from 0.5 +/- 0.1 to 0.9 +/- 0.2 mmol/l (P
< 0.05), respectively. The A-I glucose concentration difference was
abolished immediately postischemia and regained after approximately 15
min, whereas high interstitial lactate levels remained elevated
throughout the study. Subcutaneous interstitial glucose concentrations
remained unchanged during ischemia and postischemia in both groups,
whereas the interstitial lactate concentration in adipose tissue
increased during ischemia from 1.4 +/- 0.2 to 2.0 +/- 0.2 mmol/l (P <
0.05) and from 1.1 +/- 0.1 to 1.8 +/- 0.3 mmol/l (P < 0.05) in type 2
diabetic patients and control subjects, respectively. Plasma glucose
and lactate levels were unchanged in both groups during the study
period. The results show that in muscle, but not in adipose tissue,
glucose uptake is efficiently activated by ischemia in
insulin-resistant type 2 diabetic subjects, suggesting the activation
of a putative alternative pathway to the insulin signal in muscle
cells.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=10909976
"
Can above studies indirectly suggest that increased nutrients exposure
(as glucose/fats etc.) may cause loss of capillaries whereas decresed
nutrients exposure may promote new capillaties requirtments? A cause
and reason to increased or decreased effect of Insulin?

Can endothelial cells in intima,
smooth muscle cells and elastic tissue in media and connective tissues
in adventitia take water and swell/brust in hypotonic environment?


The latter is not clinically seen.


In formers?


You wouldn't be able to swim in lakes and rivers without exploding
otherwise.

Yes, as such, what about fats deposition in former's regions?

In short, can there be some defect in mirovessels which may resist or
restrict transcapillary movement of insulin? [ I now started thinking,
if such insulin movement is controlled by changes in glucose oriented
changes in tonicity of blood resulting into change in the size of
cells wall tissues(endoth. cell swelling) restricting transcaillary
movement of bigger molecules as insulin may be one reason to decresed
effect of insulin]?


Not clinically seen.

In case of endothelliul dysfunctions?

Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).
http://HeartMDPhD.com/Love

.
User: "Andrew B. Chung, MD/PhD"

Title: Re: Culprit to Insulin resistance? 24 Nov 2006 09:43:06 AM
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:

snip> > > > Whether intimal's cells swelling/inflammation can resist
insulin's

movement to extravascular tissues(glucose?)..somewhat as you told that
supply to tissues is restricted resulting arthritis?


Not clinically seen.


Pls tell me again about decreased supply due to intimal inflammation
causing arthritis?


Osteoarthritis, which is the most common arthritis affecting adults, is
likely caused by microvascular problems arising from microvascular
inflammation driven by VAT.


Whether such microvascular problem/inflammation is atherosclerosis or
by cell's swelling due to hyotonicity of blood in comparisn to
hypertonicity of vescular wall cells?


Neither.

It is obliteration of the microvasculature.


What is it?


Loss of capillaries.


Pls look at following studies[sorry bit long but important];
To add;

"..Delayed Transcapillary Transport of Insulin to Muscle Interstitial
Fluid in Obese Subjects:
In summary, the present data show for the first time that obese humans
have a delayed distribution of insulin-to-muscle interstitial fluid as
well as a slower activation of the glucose uptake rate. These data
suggest that a delayed delivery of insulin may contribute to muscle
insulin resistance in obesity.
http://diabetes.diabetesjournals.org/cgi/content/full/51/9/2742 "

": Diabetes. 2005 Jan;54(1):152-7. Links
Retraction in:
Sjostrand M, Gudbjornsdottir S, Strindberg L, Lonnroth P. Diabetes.
2005 Jul;54(7):2266.
Delayed transcapillary delivery of insulin to muscle interstitial fluid
after oral glucose load in obese subjects.
Sjostrand M, Gudbjornsdottir S, Strindberg L, Lonnroth P.
Lundberg Laboratory for Diabetes Research, Sahlgrenska University
Hospital, S-41345 Goteborg, Sweden.



Obese subjects exhibit a delay in insulin action and delivery of
insulin to muscle interstitial fluid during glucose/insulin infusion.
The aim of the present study was to follow the distribution of insulin
to skeletal muscle after an oral glucose load in obese subjects. We
conducted an oral glucose tolerance test (OGTT) in 10 lean and 10 obese
subjects (BMI 23 +/- 0.6 vs. 33 +/- 1.2 kg/m(2); P < 0.001). Insulin
measurements in muscle interstitial fluid were combined with forearm
arteriovenous catheterization and blood flow measurements. In the obese
group, interstitial insulin was significantly (35-55%) lower than
plasma insulin (P < 0.05) during the 1st h after the OGTT, whereas in
lean subjects, no significant difference was found between interstitial
and plasma insulin levels during the same time period. The permeability
surface area product for glucose, representing capillary recruitment,
increased in the lean group (P < 0.05) but not in the obese group (NS).
Obese subjects had a significantly higher plasma insulin level at
90-120 min after oral glucose (398 +/- 57 vs. 224 +/- 37 pmol/l in
control subjects; P < 0.05). The significant gradient between plasma
insulin and muscle interstitial insulin during the first hour after
OGTT suggests a slow delivery of insulin in obese subjects. The
hindered transcapillary transport of insulin may be attributable to a
defect in insulin-mediated capillary recruitment.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15616023&dopt=Abstract
"

1: Diabetes. 2000 Jul;49(7):1178-85. Links
Muscle glucose uptake is effectively activated by ischemia in type 2
diabetic subjects.
Niklasson M, Holmang A, Sjostrand M, Strindberg L, Lonnroth P.
Department of Heart and Lung Diseases, Sahlgrenska University Hospital,
Goteborg, Sweden.


It has previously been shown that Wortmannin, a phosphatidylinositol
3-kinase inhibitor, inhibits glucose transport activated by insulin but
not by ischemia, suggesting the importance of an activating mechanism
that bypasses the insulin signal. To evaluate the relevance of this
insulin-independent pathway in insulin-resistant subjects, the ability
of ischemia to stimulate glucose uptake was investigated in 9 patients
with type 2 diabetes and in 9 healthy control subjects (fasting glucose
level 9.4 +/- 0.8 vs. 5.1 +/- 0.1 mmol/l, P < 0.001, in type 2 diabetic
patients and control subjects, respectively; fasting insulin level
insulin 8.1 +/- 2.6 vs. 4.5 +/-0.7 mU/l, P < 0.05, respectively)
matched for sex, age, and BMI. Arterial plasma and interstitial
concentrations of glucose and lactate (measured by subcutaneous and
muscle microdialysis) were recorded in the forearm before, during, and
after ischemia induced locally for 20 min. During ischemia, the muscle
interstitial glucose concentration decreased significantly from 7.7 +/-
0.6 to 5.4 +/- 0.4 mmol/l (P < 0.01) and from 4.4 +/- 0.3 to 3.6 +/-
0.3 mmol/l (P < 0.05) in type 2 diabetic patients and control subjects,
respectively. The arterial-interstitial (A-I) glucose concentration
difference was 1.7 +/- 0.6 and 0.7 +/- 0.3 mmol/ at basal, and it
increased significantly to 3.5 +/- 0.7 (P < 0.01) and 1.4 +/-0.3 mmol/l
(P < 0.05) during ischemia in each group, respectively. Interstitial
lactate increased significantly during ischemia from 0.8 +/- 0.1 to 1.1
+/- 0.1 mmol/l (P < 0.05) and from 0.5 +/- 0.1 to 0.9 +/- 0.2 mmol/l (P
< 0.05), respectively. The A-I glucose concentration difference was
abolished immediately postischemia and regained after approximately 15
min, whereas high interstitial lactate levels remained elevated
throughout the study. Subcutaneous interstitial glucose concentrations
remained unchanged during ischemia and postischemia in both groups,
whereas the interstitial lactate concentration in adipose tissue
increased during ischemia from 1.4 +/- 0.2 to 2.0 +/- 0.2 mmol/l (P <
0.05) and from 1.1 +/- 0.1 to 1.8 +/- 0.3 mmol/l (P < 0.05) in type 2
diabetic patients and control subjects, respectively. Plasma glucose
and lactate levels were unchanged in both groups during the study
period. The results show that in muscle, but not in adipose tissue,
glucose uptake is efficiently activated by ischemia in
insulin-resistant type 2 diabetic subjects, suggesting the activation
of a putative alternative pathway to the insulin signal in muscle
cells.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=10909976
"

Can above studies indirectly suggest that increased nutrients exposure
(as glucose/fats etc.) may cause loss of capillaries whereas decresed
nutrients exposure may promote new capillaties requirtments? A cause
and reason to increased or decreased effect of Insulin?

The visceral adipose tissue (VAT) remains the root source of
inflammatory cytokines that promote the systemic vascular inflammation
leading to insulin resistance.

Can endothelial cells in intima,