Can this effect extravascular Insulin transport?

Kumar said:

Hello,

"Endothelial dysfunction: a comprehensive appraisal

The junction-associated actin filament system, known as FAU system, is
found in the intercellular space and its contraction and relaxation
controls the dimension of the intercellular space. In this way, it
regulates the passage of solutes and macromolecules between the blood
and the sub endothelial space. The Ca2+ concentrations, intracellular
second messenger and the common factor of the external function of
cells with intermittent or cyclic activities activate it, the energy
is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
cytokines, reactive oxygen species, thrombin, platelet activating
factor, an increase of Ca2+ concentration in ischemic conditions, ATP
exhaustion and other toxic substances, alter the functions of the
junction-associated actin filament system and allow an opening of the
intercellular space and, with that, alteration of the endothelial
permeability. The FAU system is closely related to the intercellular
adhesion molecules, especially with VE-cadherine maintaining a balance
between adhesive and contractile forces. Both cyclic adenosine mono-
phosphate (cAMP), originated through the adenylate-cyclase, and the
cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
guanylate-cyclase dependent pathway, are second messengers that
stabilize the FAU system and counteract the induction of intercellular
separation, which is done through a Ca2+-dependent calmodulin.
Nitrates, behave the same way. Protein-kinase C (PKC) activation has
the opposite effect (Figure 2.)

http://www.cardiab.com/content/5/1/4 "

Above link provided detailed information on Endothelial dysfunction.

Can it cause altered/abnormal movement of insulin to extravascular,
transcapillary target tissues, expressing somewhat insulin resistance?

Increased endothelial permeability would increase rate of insulin
delivery to the interstitium only if the permeability had been rate-
limiting.

This would increase insulin sensitivity which is not what is observed
during chronic pro-inflammatory conditions of metabolic syndrome
(MetS) caused by the presence of visceral adipose tissue (VAT).

Quoted message said:

Role of Pro-inflammatory cytokines & reactive oxygen species, which
may be relating to VAT may be brainstorming in this regard as may have
increasing vascular permeability, probably purpose may be to increase
restricted insulin's transcapillary transport.

There is no transcapillary transport of insulin restricted or not.

Insulin resistance is occurring at the cellular level.

May GOD bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."
http://HeartMDPhD.com/Love/TheTruth

MD/PhD said:

Kumar said:

Hello,

Quoted message said:

"Endothelial dysfunction: a comprehensive appraisal

Quoted message said:

The junction-associated actin filament system, known as FAU system, is
found in the intercellular space and its contraction and relaxation
controls the dimension of the intercellular space. In this way, it
regulates the passage of solutes and macromolecules between the blood
and the sub endothelial space. The Ca2+ concentrations, intracellular
second messenger and the common factor of the external function of
cells with intermittent or cyclic activities activate it, the energy
is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
cytokines, reactive oxygen species, thrombin, platelet activating
factor, an increase of Ca2+ concentration in ischemic conditions, ATP
exhaustion and other toxic substances, alter the functions of the
junction-associated actin filament system and allow an opening of the
intercellular space and, with that, alteration of the endothelial
permeability. The FAU system is closely related to the intercellular
adhesion molecules, especially with VE-cadherine maintaining a balance
between adhesive and contractile forces. Both cyclic adenosine mono-
phosphate (cAMP), originated through the adenylate-cyclase, and the
cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
guanylate-cyclase dependent pathway, are second messengers that
stabilize the FAU system and counteract the induction of intercellular
separation, which is done through a Ca2+-dependent calmodulin.
Nitrates, behave the same way. Protein-kinase C (PKC) activation has
the opposite effect (Figure 2.)

Quoted message said:

cardiab.com4"Open ↗

Quoted message said:

Above link provided detailed information on Endothelial dysfunction.

Quoted message said:

Can it cause altered/abnormal movement of insulin to extravascular,
transcapillary target tissues, expressing somewhat insulin resistance?

Increased endothelial permeability would increase rate of insulin
delivery to the interstitium only if the permeability had been rate-
limiting.

Decreased endothelial permeability due to opposing reasons or end.
cells swelling?

Btw, whether ionized calcium increases endothelial permeability as per
above link?

Quoted message said:

This would increase insulin sensitivity which is not what is observed
during chronic pro-inflammatory conditions of metabolic syndrome
(MetS) caused by the presence of visceral adipose tissue (VAT).

Such inflammatory conditions can be meant to increase previous
decreased endothelial permeability i.e. trying towards normal?

Quoted message said:

Quoted message said:

Role of Pro-inflammatory cytokines & reactive oxygen species, which
may be relating to VAT may be brainstorming in this regard as may have
increasing vascular permeability, probably purpose may be to increase
restricted insulin's transcapillary transport.

There is no transcapillary transport of insulin restricted or not.

Why there can't be endothelial dysfunction/decreased permeability
reason to extravascular movement of insulin which may decreases 0.2
vascular permeability to insulin as per following reason or other
reasonings of endo. dysfunctions as indicated on above link in detail;

T"he junction-associated actin filament system, known as FAU system,
is
found in the intercellular space and its contraction and relaxation
controls the dimension of the intercellular space. In this way, it
regulates the passage of solutes and macromolecules between the blood
and the sub endothelial space."

Quoted message said:

Insulin resistance is occurring at the cellular level.

But still true reasonings of IR is yet un-understood fully? So other
possibilities can be thought?

Quoted message said:

May GOD bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhDhttp://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."http://HeartMDPhD.com/Love/TheTruth- Hide quoted text -

- Show quoted text -

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar said:

Hello,

Quoted message said:

"Endothelial dysfunction: a comprehensive appraisal

Quoted message said:

The junction-associated actin filament system, known as FAU system, is
found in the intercellular space and its contraction and relaxation
controls the dimension of the intercellular space. In this way, it
regulates the passage of solutes and macromolecules between the blood
and the sub endothelial space. The Ca2+ concentrations, intracellular
second messenger and the common factor of the external function of
cells with intermittent or cyclic activities activate it, the energy
is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
cytokines, reactive oxygen species, thrombin, platelet activating
factor, an increase of Ca2+ concentration in ischemic conditions, ATP
exhaustion and other toxic substances, alter the functions of the
junction-associated actin filament system and allow an opening of the
intercellular space and, with that, alteration of the endothelial
permeability. The FAU system is closely related to the intercellular
adhesion molecules, especially with VE-cadherine maintaining a balance
between adhesive and contractile forces. Both cyclic adenosine mono-
phosphate (cAMP), originated through the adenylate-cyclase, and the
cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
guanylate-cyclase dependent pathway, are second messengers that
stabilize the FAU system and counteract the induction of intercellular
separation, which is done through a Ca2+-dependent calmodulin.
Nitrates, behave the same way. Protein-kinase C (PKC) activation has
the opposite effect (Figure 2.)

Quoted message said:

cardiab.com4"Open ↗

Quoted message said:

Above link provided detailed information on Endothelial dysfunction.

Quoted message said:

Can it cause altered/abnormal movement of insulin to extravascular,
transcapillary target tissues, expressing somewhat insulin resistance?

Increased endothelial permeability would increase rate of insulin
delivery to the interstitium only if the permeability had been rate-
limiting.

Decreased endothelial permeability due to opposing reasons or end.
cells swelling?

Compared to normal endothelial permeability.

Quoted message said:

Btw, whether ionized calcium increases endothelial permeability as per
above link?

It does.

Quoted message said:

Quoted message said:

This would increase insulin sensitivity which is not what is observed
during chronic pro-inflammatory conditions of metabolic syndrome
(MetS) caused by the presence of visceral adipose tissue (VAT).

Such inflammatory conditions can be meant to increase previous
decreased endothelial permeability i.e. trying towards normal?

Quoted message said:

Quoted message said:

Role of Pro-inflammatory cytokines & reactive oxygen species, which
may be relating to VAT may be brainstorming in this regard as may have
increasing vascular permeability, probably purpose may be to increase
restricted insulin's transcapillary transport.

There is no transcapillary transport of insulin restricted or not.

Why there can't be endothelial dysfunction/decreased permeability
reason to extravascular movement of insulin which may decreases 0.2
vascular permeability to insulin as per following reason or other
reasonings of endo. dysfunctions as indicated on above link in detail;

T"he junction-associated actin filament system, known as FAU system,
is
found in the intercellular space and its contraction and relaxation
controls the dimension of the intercellular space. In this way, it
regulates the passage of solutes and macromolecules between the blood
and the sub endothelial space."

Regulation of "rates of passage (diffusion)" is not transport.

Quoted message said:

Quoted message said:

Insulin resistance is occurring at the cellular level.

But still true reasonings of IR is yet un-understood fully? So other
possibilities can be thought?

Actually insulin resistance is a well understood consequence of
inflammation arising because of visceral adipose tissue (VAT).

A recent small study to illustrate this understanding:

http://tinyurl.com/2gwnxp

May GOD bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."
http://HeartMDPhD.com/Love/TheTruth

MD/PhD said:

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar wrote:

Quoted message said:

Quoted message said:

> Hello,

Quoted message said:

Quoted message said:

> "Endothelial dysfunction: a comprehensive appraisal

Quoted message said:

Quoted message said:

> The junction-associated actin filament system, known as FAU system, is
> found in the intercellular space and its contraction and relaxation
> controls the dimension of the intercellular space. In this way, it
> regulates the passage of solutes and macromolecules between the blood
> and the sub endothelial space. The Ca2+ concentrations, intracellular
> second messenger and the common factor of the external function of
> cells with intermittent or cyclic activities activate it, the energy
> is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
> cytokines, reactive oxygen species, thrombin, platelet activating
> factor, an increase of Ca2+ concentration in ischemic conditions, ATP
> exhaustion and other toxic substances, alter the functions of the
> junction-associated actin filament system and allow an opening of the
> intercellular space and, with that, alteration of the endothelial
> permeability. The FAU system is closely related to the intercellular
> adhesion molecules, especially with VE-cadherine maintaining a balance
> between adhesive and contractile forces. Both cyclic adenosine mono-
> phosphate (cAMP), originated through the adenylate-cyclase, and the
> cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
> guanylate-cyclase dependent pathway, are second messengers that
> stabilize the FAU system and counteract the induction of intercellular
> separation, which is done through a Ca2+-dependent calmodulin.
> Nitrates, behave the same way. Protein-kinase C (PKC) activation has
> the opposite effect (Figure 2.)

Quoted message said:

Quoted message said:

>http://www.cardiab.com/content/5/1/4"

Quoted message said:

Quoted message said:

> Above link provided detailed information on Endothelial dysfunction.

Quoted message said:

Quoted message said:

> Can it cause altered/abnormal movement of insulin to extravascular,
> transcapillary target tissues, expressing somewhat insulin resistance?

Quoted message said:

Quoted message said:

Increased endothelial permeability would increase rate of insulin
delivery to the interstitium only if the permeability had been rate-
limiting.

Quoted message said:

Decreased endothelial permeability due to opposing reasons or end.
cells swelling?

Compared to normal endothelial permeability.

Quoted message said:

Quoted message said:

Btw, whether ionized calcium increases endothelial permeability as per
above link?

It does.

Means, diabetics who have low level of ionized calcium in their blood
can have low endo. permeabilty and chances of lesser insulin movement
to extravascular tissues resulting hyperglycemia?

Quoted message said:

Quoted message said:

Quoted message said:

This would increase insulin sensitivity which is not what is observed
during chronic pro-inflammatory conditions of metabolic syndrome
(MetS) caused by the presence of visceral adipose tissue (VAT).

Such inflammatory conditions can be meant to increase previous
decreased endothelial permeability i.e. trying towards normal?

Quoted message said:

> Role of Pro-inflammatory cytokines & reactive oxygen species, which
> may be relating to VAT may be brainstorming in this regard as may have
> increasing vascular permeability, probably purpose may be to increase
> restricted insulin's transcapillary transport.

Quoted message said:

Quoted message said:

There is no transcapillary transport of insulin restricted or not.

Quoted message said:

Why there can't be endothelial dysfunction/decreased permeability
reason to extravascular movement of insulin which may decreases 0.2
vascular permeability to insulin as per following reason or other
reasonings of endo. dysfunctions as indicated on above link in detail;

Quoted message said:

T"he junction-associated actin filament system, known as FAU system,
is
found in the intercellular space and its contraction and relaxation
controls the dimension of the intercellular space. In this way, it
regulates the passage of solutes and macromolecules between the blood
and the sub endothelial space."

Regulation of "rates of passage (diffusion)" is not transport.

You may call it insulin movement to extravascular target cells? Now
pls reply previous question?

Quoted message said:

Quoted message said:

Quoted message said:

Insulin resistance is occurring at the cellular level.

Quoted message said:

But still true reasonings of IR is yet un-understood fully? So other
possibilities can be thought?

Actually insulin resistance is a well understood consequence of
inflammation arising because of visceral adipose tissue (VAT).

How it interfere in insulin senstivity to target cells?

Quoted message said:

A recent small study to illustrate this understanding:

http://tinyurl.com/2gwnxp

May GOD bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhDhttp://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."http://HeartMDPhD.com/Love/TheTruth- Hide quoted text -

- Show quoted text -- Hide quoted text -

- Show quoted text -

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar said:

Andrew, in the Holy Spirit, boldly wrote:
> convicted neighbor Kumar wrote:

Quoted message said:

> > Hello,

Quoted message said:

> > "Endothelial dysfunction: a comprehensive appraisal

Quoted message said:

> > The junction-associated actin filament system, known as FAU system, is
> > found in the intercellular space and its contraction and relaxation
> > controls the dimension of the intercellular space. In this way, it
> > regulates the passage of solutes and macromolecules between the blood
> > and the sub endothelial space. The Ca2+ concentrations, intracellular
> > second messenger and the common factor of the external function of
> > cells with intermittent or cyclic activities activate it, the energy
> > is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
> > cytokines, reactive oxygen species, thrombin, platelet activating
> > factor, an increase of Ca2+ concentration in ischemic conditions, ATP
> > exhaustion and other toxic substances, alter the functions of the
> > junction-associated actin filament system and allow an opening of the
> > intercellular space and, with that, alteration of the endothelial
> > permeability. The FAU system is closely related to the intercellular
> > adhesion molecules, especially with VE-cadherine maintaining a balance
> > between adhesive and contractile forces. Both cyclic adenosine mono-
> > phosphate (cAMP), originated through the adenylate-cyclase, and the
> > cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
> > guanylate-cyclase dependent pathway, are second messengers that
> > stabilize the FAU system and counteract the induction of intercellular
> > separation, which is done through a Ca2+-dependent calmodulin.
> > Nitrates, behave the same way. Protein-kinase C (PKC) activation has
> > the opposite effect (Figure 2.)

Quoted message said:

> >http://www.cardiab.com/content/5/1/4"

Quoted message said:

> > Above link provided detailed information on Endothelial dysfunction.

Quoted message said:

> > Can it cause altered/abnormal movement of insulin to extravascular,
> > transcapillary target tissues, expressing somewhat insulin resistance?

Quoted message said:

> Increased endothelial permeability would increase rate of insulin
> delivery to the interstitium only if the permeability had been rate-
> limiting.

Quoted message said:

Decreased endothelial permeability due to opposing reasons or end.
cells swelling?

Compared to normal endothelial permeability.

Quoted message said:

Quoted message said:

Btw, whether ionized calcium increases endothelial permeability as per
above link?

It does.

Means, diabetics who have low level of ionized calcium in their blood
can have low endo. permeabilty and chances of lesser insulin movement
to extravascular tissues resulting hyperglycemia?

Not clinically seen.

Slower rates of diffusion does not necessarily mean less insulin gets
to target tissues.

Quoted message said:

Quoted message said:

Quoted message said:

> This would increase insulin sensitivity which is not what is observed
> during chronic pro-inflammatory conditions of metabolic syndrome
> (MetS) caused by the presence of visceral adipose tissue (VAT).
Such inflammatory conditions can be meant to increase previous
decreased endothelial permeability i.e. trying towards normal?
> > Role of Pro-inflammatory cytokines & reactive oxygen species, which
> > may be relating to VAT may be brainstorming in this regard as may have
> > increasing vascular permeability, probably purpose may be to increase
> > restricted insulin's transcapillary transport.

Quoted message said:

> There is no transcapillary transport of insulin restricted or not.

Quoted message said:

Why there can't be endothelial dysfunction/decreased permeability
reason to extravascular movement of insulin which may decreases 0.2
vascular permeability to insulin as per following reason or other
reasonings of endo. dysfunctions as indicated on above link in detail;

Quoted message said:

T"he junction-associated actin filament system, known as FAU system,
is
found in the intercellular space and its contraction and relaxation
controls the dimension of the intercellular space. In this way, it
regulates the passage of solutes and macromolecules between the blood
and the sub endothelial space."

Regulation of "rates of passage (diffusion)" is not transport.

You may call it insulin movement to extravascular target cells? Now
pls reply previous question?

It is simply diffusion which is movement from higher concentration to
lower concentration.

Quoted message said:

Quoted message said:

Quoted message said:

> Insulin resistance is occurring at the cellular level.

Quoted message said:

But still true reasonings of IR is yet un-understood fully? So other
possibilities can be thought?

Actually insulin resistance is a well understood consequence of
inflammation arising because of visceral adipose tissue (VAT).

Quoted message said:

How it interfere in insulin senstivity to target cells?

Results in less insulin receptors and less second messenger response
with receptor activation.

Quoted message said:

Quoted message said:

A recent small study to illustrate this understanding:

http://tinyurl.com/2gwnxp

May GOD bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."
http://HeartMDPhD.com/Love/TheTruth

MD/PhD said:

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar wrote:
> Andrew, in the Holy Spirit, boldly wrote:
> > convicted neighbor Kumar wrote:

Quoted message said:

Quoted message said:

> > > Hello,

Quoted message said:

Quoted message said:

> > > "Endothelial dysfunction: a comprehensive appraisal

Quoted message said:

Quoted message said:

> > > The junction-associated actin filament system, known as FAU system, is
> > > found in the intercellular space and its contraction and relaxation
> > > controls the dimension of the intercellular space. In this way, it
> > > regulates the passage of solutes and macromolecules between the blood
> > > and the sub endothelial space. The Ca2+ concentrations, intracellular
> > > second messenger and the common factor of the external function of
> > > cells with intermittent or cyclic activities activate it, the energy
> > > is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
> > > cytokines, reactive oxygen species, thrombin, platelet activating
> > > factor, an increase of Ca2+ concentration in ischemic conditions, ATP
> > > exhaustion and other toxic substances, alter the functions of the
> > > junction-associated actin filament system and allow an opening of the
> > > intercellular space and, with that, alteration of the endothelial
> > > permeability. The FAU system is closely related to the intercellular
> > > adhesion molecules, especially with VE-cadherine maintaining a balance
> > > between adhesive and contractile forces. Both cyclic adenosine mono-
> > > phosphate (cAMP), originated through the adenylate-cyclase, and the
> > > cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
> > > guanylate-cyclase dependent pathway, are second messengers that
> > > stabilize the FAU system and counteract the induction of intercellular
> > > separation, which is done through a Ca2+-dependent calmodulin.
> > > Nitrates, behave the same way. Protein-kinase C (PKC) activation has
> > > the opposite effect (Figure 2.)

Quoted message said:

Quoted message said:

> > >http://www.cardiab.com/content/5/1/4"

Quoted message said:

Quoted message said:

> > > Above link provided detailed information on Endothelial dysfunction.

Quoted message said:

Quoted message said:

> > > Can it cause altered/abnormal movement of insulin to extravascular,
> > > transcapillary target tissues, expressing somewhat insulin resistance?

Quoted message said:

Quoted message said:

> > Increased endothelial permeability would increase rate of insulin
> > delivery to the interstitium only if the permeability had been rate-
> > limiting.

Quoted message said:

Quoted message said:

> Decreased endothelial permeability due to opposing reasons or end.
> cells swelling?

Quoted message said:

Quoted message said:

Compared to normal endothelial permeability.

Quoted message said:

Quoted message said:

> Btw, whether ionized calcium increases endothelial permeability as per
> above link?

Quoted message said:

Quoted message said:

It does.

Quoted message said:

Means, diabetics who have low level of ionized calcium in their blood
can have low endo. permeabilty and chances of lesser insulin movement
to extravascular tissues resulting hyperglycemia?

Not clinically seen.

At later stages, calcium levels decreases?

Quoted message said:

Slower rates of diffusion does not necessarily mean less insulin gets
to target tissues.

Insulin has short half life of just 6 minutes. It should be possible
on altered cap.. pores dimentions?

Quoted message said:

Quoted message said:

Quoted message said:

> > This would increase insulin sensitivity which is not what is observed
> > during chronic pro-inflammatory conditions of metabolic syndrome
> > (MetS) caused by the presence of visceral adipose tissue (VAT).
> Such inflammatory conditions can be meant to increase previous
> decreased endothelial permeability i.e. trying towards normal?
> > > Role of Pro-inflammatory cytokines & reactive oxygen species, which
> > > may be relating to VAT may be brainstorming in this regard as may have
> > > increasing vascular permeability, probably purpose may be to increase
> > > restricted insulin's transcapillary transport.

Quoted message said:

Quoted message said:

> > There is no transcapillary transport of insulin restricted or not.

Quoted message said:

Quoted message said:

> Why there can't be endothelial dysfunction/decreased permeability
> reason to extravascular movement of insulin which may decreases 0.2
> vascular permeability to insulin as per following reason or other
> reasonings of endo. dysfunctions as indicated on above link in detail;

Quoted message said:

Quoted message said:

> T"he junction-associated actin filament system, known as FAU system,
> is
> found in the intercellular space and its contraction and relaxation
> controls the dimension of the intercellular space. In this way, it
> regulates the passage of solutes and macromolecules between the blood
> and the sub endothelial space."

Quoted message said:

Quoted message said:

Regulation of "rates of passage (diffusion)" is not transport.

Quoted message said:

You may call it insulin movement to extravascular target cells? Now
pls reply previous question?

It is simply diffusion which is movement from higher concentration to
lower concentration.

Is it of insulin's higher/lower concentration or insulin's diffusion
is effected by others?

Quoted message said:

Quoted message said:

Quoted message said:

> > Insulin resistance is occurring at the cellular level.

Quoted message said:

Quoted message said:

> But still true reasonings of IR is yet un-understood fully? So other
> possibilities can be thought?

Quoted message said:

Quoted message said:

Actually insulin resistance is a well understood consequence of
inflammation arising because of visceral adipose tissue (VAT).

How it interfere in insulin senstivity to target cells?

Results in less insulin receptors and less second messenger response
with receptor activation.

Means, VAT oriented inflammation causes lesser or down regulation of
insulin's receptors?

Quoted message said:

Quoted message said:

Quoted message said:

A recent small study to illustrate this understanding:

Quoted message said:

Quoted message said:

http://tinyurl.com/2gwnxp

May GOD bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhDhttp://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."http://HeartMDPhD.com/Love/TheTruth- Hide quoted text -

- Show quoted text -- Hide quoted text -

- Show quoted text -

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar said:

Andrew, in the Holy Spirit, boldly wrote:
> convicted neighbor Kumar wrote:
> > Andrew, in the Holy Spirit, boldly wrote:
> > > convicted neighbor Kumar wrote:

Quoted message said:

> > > > Hello,

Quoted message said:

> > > > "Endothelial dysfunction: a comprehensive appraisal

Quoted message said:

> > > > The junction-associated actin filament system, known as FAU system, is
> > > > found in the intercellular space and its contraction and relaxation
> > > > controls the dimension of the intercellular space. In this way, it
> > > > regulates the passage of solutes and macromolecules between the blood
> > > > and the sub endothelial space. The Ca2+ concentrations, intracellular
> > > > second messenger and the common factor of the external function of
> > > > cells with intermittent or cyclic activities activate it, the energy
> > > > is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
> > > > cytokines, reactive oxygen species, thrombin, platelet activating
> > > > factor, an increase of Ca2+ concentration in ischemic conditions, ATP
> > > > exhaustion and other toxic substances, alter the functions of the
> > > > junction-associated actin filament system and allow an opening of the
> > > > intercellular space and, with that, alteration of the endothelial
> > > > permeability. The FAU system is closely related to the intercellular
> > > > adhesion molecules, especially with VE-cadherine maintaining a balance
> > > > between adhesive and contractile forces. Both cyclic adenosine mono-
> > > > phosphate (cAMP), originated through the adenylate-cyclase, and the
> > > > cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
> > > > guanylate-cyclase dependent pathway, are second messengers that
> > > > stabilize the FAU system and counteract the induction of intercellular
> > > > separation, which is done through a Ca2+-dependent calmodulin.
> > > > Nitrates, behave the same way. Protein-kinase C (PKC) activation has
> > > > the opposite effect (Figure 2.)

Quoted message said:

> > > >http://www.cardiab.com/content/5/1/4"

Quoted message said:

> > > > Above link provided detailed information on Endothelial dysfunction.

Quoted message said:

> > > > Can it cause altered/abnormal movement of insulin to extravascular,
> > > > transcapillary target tissues, expressing somewhat insulin resistance?

Quoted message said:

> > > Increased endothelial permeability would increase rate of insulin
> > > delivery to the interstitium only if the permeability had been rate-
> > > limiting.

Quoted message said:

> > Decreased endothelial permeability due to opposing reasons or end.
> > cells swelling?

Quoted message said:

> Compared to normal endothelial permeability.

Quoted message said:

> > Btw, whether ionized calcium increases endothelial permeability as per
> > above link?

Quoted message said:

> It does.

Quoted message said:

Means, diabetics who have low level of ionized calcium in their blood
can have low endo. permeabilty and chances of lesser insulin movement
to extravascular tissues resulting hyperglycemia?

Not clinically seen.

At later stages, calcium levels decreases?

Hypocalcemia is not a characteristic of having diabetes even at later
stages.

Quoted message said:

Quoted message said:

Slower rates of diffusion does not necessarily mean less insulin gets
to target tissues.

Insulin has short half life of just 6 minutes. It should be possible
on altered cap.. pores dimentions?

Possible but not clinically observed.

Quoted message said:

Quoted message said:

Quoted message said:

> > > This would increase insulin sensitivity which is not what is observed
> > > during chronic pro-inflammatory conditions of metabolic syndrome
> > > (MetS) caused by the presence of visceral adipose tissue (VAT).
> > Such inflammatory conditions can be meant to increase previous
> > decreased endothelial permeability i.e. trying towards normal?
> > > > Role of Pro-inflammatory cytokines & reactive oxygen species, which
> > > > may be relating to VAT may be brainstorming in this regard as may have
> > > > increasing vascular permeability, probably purpose may be to increase
> > > > restricted insulin's transcapillary transport.

Quoted message said:

> > > There is no transcapillary transport of insulin restricted or not.

Quoted message said:

> > Why there can't be endothelial dysfunction/decreased permeability
> > reason to extravascular movement of insulin which may decreases 0.2
> > vascular permeability to insulin as per following reason or other
> > reasonings of endo. dysfunctions as indicated on above link in detail;

Quoted message said:

> > T"he junction-associated actin filament system, known as FAU system,
> > is
> > found in the intercellular space and its contraction and relaxation
> > controls the dimension of the intercellular space. In this way, it
> > regulates the passage of solutes and macromolecules between the blood
> > and the sub endothelial space."

Quoted message said:

> Regulation of "rates of passage (diffusion)" is not transport.

Quoted message said:

You may call it insulin movement to extravascular target cells? Now
pls reply previous question?

It is simply diffusion which is movement from higher concentration to
lower concentration.

Is it of insulin's higher/lower concentration or insulin's diffusion
is effected by others?

Diffusion is the process by which molecules disperse from higher to
lower concentration. The rate of diffusion is dependent on the size
of the molecules and their respective kinetic energies.

Quoted message said:

Quoted message said:

Quoted message said:

> > > Insulin resistance is occurring at the cellular level.

Quoted message said:

> > But still true reasonings of IR is yet un-understood fully? So other
> > possibilities can be thought?

Quoted message said:

> Actually insulin resistance is a well understood consequence of
> inflammation arising because of visceral adipose tissue (VAT).
How it interfere in insulin senstivity to target cells?

Results in less insulin receptors and less second messenger response
with receptor activation.

Means, VAT oriented inflammation causes lesser or down regulation of
insulin's receptors?

And possible impairment of receptor response (damaged receptors).

May GOD bless you in HIS mighty way.

You will know when this happens because you will feel hungrier.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."
http://HeartMDPhD.com/Love/TheTruth

MD/PhD said:

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar wrote:
> Andrew, in the Holy Spirit, boldly wrote:
> > convicted neighbor Kumar wrote:
> > > Andrew, in the Holy Spirit, boldly wrote:
> > > > convicted neighbor Kumar wrote:

Quoted message said:

Quoted message said:

> > > > > Hello,

Quoted message said:

Quoted message said:

> > > > > "Endothelial dysfunction: a comprehensive appraisal

Quoted message said:

Quoted message said:

> > > > > The junction-associated actin filament system, known as FAU system, is
> > > > > found in the intercellular space and its contraction and relaxation
> > > > > controls the dimension of the intercellular space. In this way, it
> > > > > regulates the passage of solutes and macromolecules between the blood
> > > > > and the sub endothelial space. The Ca2+ concentrations, intracellular
> > > > > second messenger and the common factor of the external function of
> > > > > cells with intermittent or cyclic activities activate it, the energy
> > > > > is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
> > > > > cytokines, reactive oxygen species, thrombin, platelet activating
> > > > > factor, an increase of Ca2+ concentration in ischemic conditions, ATP
> > > > > exhaustion and other toxic substances, alter the functions of the
> > > > > junction-associated actin filament system and allow an opening of the
> > > > > intercellular space and, with that, alteration of the endothelial
> > > > > permeability. The FAU system is closely related to the intercellular
> > > > > adhesion molecules, especially with VE-cadherine maintaining a balance
> > > > > between adhesive and contractile forces. Both cyclic adenosine mono-
> > > > > phosphate (cAMP), originated through the adenylate-cyclase, and the
> > > > > cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
> > > > > guanylate-cyclase dependent pathway, are second messengers that
> > > > > stabilize the FAU system and counteract the induction of intercellular
> > > > > separation, which is done through a Ca2+-dependent calmodulin.
> > > > > Nitrates, behave the same way. Protein-kinase C (PKC) activation has
> > > > > the opposite effect (Figure 2.)

Quoted message said:

Quoted message said:

> > > > >http://www.cardiab.com/content/5/1/4"

Quoted message said:

Quoted message said:

> > > > > Above link provided detailed information on Endothelial dysfunction.

Quoted message said:

Quoted message said:

> > > > > Can it cause altered/abnormal movement of insulin to extravascular,
> > > > > transcapillary target tissues, expressing somewhat insulin resistance?

Quoted message said:

Quoted message said:

> > > > Increased endothelial permeability would increase rate of insulin
> > > > delivery to the interstitium only if the permeability had been rate-
> > > > limiting.

Quoted message said:

Quoted message said:

> > > Decreased endothelial permeability due to opposing reasons or end.
> > > cells swelling?

Quoted message said:

Quoted message said:

> > Compared to normal endothelial permeability.

Quoted message said:

Quoted message said:

> > > Btw, whether ionized calcium increases endothelial permeability as per
> > > above link?

Quoted message said:

Quoted message said:

> > It does.

Quoted message said:

Quoted message said:

> Means, diabetics who have low level of ionized calcium in their blood
> can have low endo. permeabilty and chances of lesser insulin movement
> to extravascular tissues resulting hyperglycemia?

Quoted message said:

Quoted message said:

Not clinically seen.

Quoted message said:

At later stages, calcium levels decreases?

Hypocalcemia is not a characteristic of having diabetes even at later
stages.

Will lower levels of calcium not decrease endothelial permeability ?
If yes, it can be reason to hyperglycemia not hypoglycmia?

Quoted message said:

Quoted message said:

Quoted message said:

Slower rates of diffusion does not necessarily mean less insulin gets
to target tissues.

Quoted message said:

Insulin has short half life of just 6 minutes. It should be possible
on altered cap.. pores dimentions?

Possible but not clinically observed.

Can you provide some links where it is studied?

Quoted message said:

Quoted message said:

Quoted message said:

> > > > This would increase insulin sensitivity which is not what is observed
> > > > during chronic pro-inflammatory conditions of metabolic syndrome
> > > > (MetS) caused by the presence of visceral adipose tissue (VAT).
> > > Such inflammatory conditions can be meant to increase previous
> > > decreased endothelial permeability i.e. trying towards normal?
> > > > > Role of Pro-inflammatory cytokines & reactive oxygen species, which
> > > > > may be relating to VAT may be brainstorming in this regard as may have
> > > > > increasing vascular permeability, probably purpose may be to increase
> > > > > restricted insulin's transcapillary transport.

Quoted message said:

Quoted message said:

> > > > There is no transcapillary transport of insulin restricted or not.

Quoted message said:

Quoted message said:

> > > Why there can't be endothelial dysfunction/decreased permeability
> > > reason to extravascular movement of insulin which may decreases 0.2
> > > vascular permeability to insulin as per following reason or other
> > > reasonings of endo. dysfunctions as indicated on above link in detail;

Quoted message said:

Quoted message said:

> > > T"he junction-associated actin filament system, known as FAU system,
> > > is
> > > found in the intercellular space and its contraction and relaxation
> > > controls the dimension of the intercellular space. In this way, it
> > > regulates the passage of solutes and macromolecules between the blood
> > > and the sub endothelial space."

Regulation of "rates of passage (diffusion)" is not transport.

Btw, if diffusion is not a passive transport?

Quoted message said:

Quoted message said:

Quoted message said:

> You may call it insulin movement to extravascular target cells? Now
> pls reply previous question?

Quoted message said:

Quoted message said:

It is simply diffusion which is movement from higher concentration to
lower concentration.

Quoted message said:

Is it of insulin's higher/lower concentration or insulin's diffusion
is effected by others?

Diffusion is the process by which molecules disperse from higher to
lower concentration. The rate of diffusion is dependent on the size
of the molecules and their respective kinetic energies.

Higher to lower concentration of which molecules in case of insulin's
diffusion?

Quoted message said:

Quoted message said:

Quoted message said:

> > > > Insulin resistance is occurring at the cellular level.

Quoted message said:

Quoted message said:

> > > But still true reasonings of IR is yet un-understood fully? So other
> > > possibilities can be thought?

Quoted message said:

Quoted message said:

> > Actually insulin resistance is a well understood consequence of
> > inflammation arising because of visceral adipose tissue (VAT).
> How it interfere in insulin senstivity to target cells?

Quoted message said:

Quoted message said:

Results in less insulin receptors and less second messenger response
with receptor activation.

Means, VAT oriented inflammation causes lesser or down regulation of
insulin's receptors?

And possible impairment of receptor response (damaged receptors).

Will VAT oriented inflammation effect all extravascular target cells?

Quoted message said:

May GOD bless you in HIS mighty way.

You will know when this happens because you will feel hungrier.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhDhttp://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."http://HeartMDPhD.com/Love/TheTruth- Hide quoted text -

- Show quoted text -- Hide quoted text -

- Show quoted text -

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar said:

Andrew, in the Holy Spirit, boldly wrote:
> convicted neighbor Kumar wrote:
> > Andrew, in the Holy Spirit, boldly wrote:
> > > convicted neighbor Kumar wrote:
> > > > Andrew, in the Holy Spirit, boldly wrote:
> > > > > convicted neighbor Kumar wrote:

Quoted message said:

> > > > > > Hello,

Quoted message said:

> > > > > > "Endothelial dysfunction: a comprehensive appraisal

Quoted message said:

> > > > > > The junction-associated actin filament system, known as FAU system, is
> > > > > > found in the intercellular space and its contraction and relaxation
> > > > > > controls the dimension of the intercellular space. In this way, it
> > > > > > regulates the passage of solutes and macromolecules between the blood
> > > > > > and the sub endothelial space. The Ca2+ concentrations, intracellular
> > > > > > second messenger and the common factor of the external function of
> > > > > > cells with intermittent or cyclic activities activate it, the energy
> > > > > > is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
> > > > > > cytokines, reactive oxygen species, thrombin, platelet activating
> > > > > > factor, an increase of Ca2+ concentration in ischemic conditions, ATP
> > > > > > exhaustion and other toxic substances, alter the functions of the
> > > > > > junction-associated actin filament system and allow an opening of the
> > > > > > intercellular space and, with that, alteration of the endothelial
> > > > > > permeability. The FAU system is closely related to the intercellular
> > > > > > adhesion molecules, especially with VE-cadherine maintaining a balance
> > > > > > between adhesive and contractile forces. Both cyclic adenosine mono-
> > > > > > phosphate (cAMP), originated through the adenylate-cyclase, and the
> > > > > > cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
> > > > > > guanylate-cyclase dependent pathway, are second messengers that
> > > > > > stabilize the FAU system and counteract the induction of intercellular
> > > > > > separation, which is done through a Ca2+-dependent calmodulin.
> > > > > > Nitrates, behave the same way. Protein-kinase C (PKC) activation has
> > > > > > the opposite effect (Figure 2.)

Quoted message said:

> > > > > >http://www.cardiab.com/content/5/1/4"

Quoted message said:

> > > > > > Above link provided detailed information on Endothelial dysfunction.

Quoted message said:

> > > > > > Can it cause altered/abnormal movement of insulin to extravascular,
> > > > > > transcapillary target tissues, expressing somewhat insulin resistance?

Quoted message said:

> > > > > Increased endothelial permeability would increase rate of insulin
> > > > > delivery to the interstitium only if the permeability had been rate-
> > > > > limiting.

Quoted message said:

> > > > Decreased endothelial permeability due to opposing reasons or end.
> > > > cells swelling?

Quoted message said:

> > > Compared to normal endothelial permeability.

Quoted message said:

> > > > Btw, whether ionized calcium increases endothelial permeability as per
> > > > above link?

Quoted message said:

> > > It does.

Quoted message said:

> > Means, diabetics who have low level of ionized calcium in their blood
> > can have low endo. permeabilty and chances of lesser insulin movement
> > to extravascular tissues resulting hyperglycemia?

Quoted message said:

> Not clinically seen.

Quoted message said:

At later stages, calcium levels decreases?

Hypocalcemia is not a characteristic of having diabetes even at later
stages.

Will lower levels of calcium not decrease endothelial permeability ?

Possibly.

Quoted message said:

If yes, it can be reason to hyperglycemia not hypoglycmia?

Reduced endothelial permeabilty has not been a clinically observed
cause of hyperglycemia.

Quoted message said:

Quoted message said:

Quoted message said:

> Slower rates of diffusion does not necessarily mean less insulin gets
> to target tissues.

Quoted message said:

Insulin has short half life of just 6 minutes. It should be possible
on altered cap.. pores dimentions?

Possible but not clinically observed.

Can you provide some links where it is studied?

As far as I know, it has not been studied.

Clinical research starts with clinical observations.

This logically follows from understanding the "scientific method."

No observations ==> no predictions ==> no experiments.

Quoted message said:

Quoted message said:

Quoted message said:

> > > > > This would increase insulin sensitivity which is not what is observed
> > > > > during chronic pro-inflammatory conditions of metabolic syndrome
> > > > > (MetS) caused by the presence of visceral adipose tissue (VAT).
> > > > Such inflammatory conditions can be meant to increase previous
> > > > decreased endothelial permeability i.e. trying towards normal?
> > > > > > Role of Pro-inflammatory cytokines & reactive oxygen species, which
> > > > > > may be relating to VAT may be brainstorming in this regard as may have
> > > > > > increasing vascular permeability, probably purpose may be to increase
> > > > > > restricted insulin's transcapillary transport.

Quoted message said:

> > > > > There is no transcapillary transport of insulin restricted or not.

Quoted message said:

> > > > Why there can't be endothelial dysfunction/decreased permeability
> > > > reason to extravascular movement of insulin which may decreases 0.2
> > > > vascular permeability to insulin as per following reason or other
> > > > reasonings of endo. dysfunctions as indicated on above link in detail;

Quoted message said:

> > > > T"he junction-associated actin filament system, known as FAU system,
> > > > is
> > > > found in the intercellular space and its contraction and relaxation
> > > > controls the dimension of the intercellular space. In this way, it
> > > > regulates the passage of solutes and macromolecules between the blood
> > > > and the sub endothelial space."

Regulation of "rates of passage (diffusion)" is not transport.

Quoted message said:

Btw, if diffusion is not a passive transport?

Diffusion is not passive transport.

Quoted message said:

Quoted message said:

Quoted message said:

> > You may call it insulin movement to extravascular target cells? Now
> > pls reply previous question?

Quoted message said:

> It is simply diffusion which is movement from higher concentration to
> lower concentration.

Quoted message said:

Is it of insulin's higher/lower concentration or insulin's diffusion
is effected by others?

Diffusion is the process by which molecules disperse from higher to
lower concentration. The rate of diffusion is dependent on the size
of the molecules and their respective kinetic energies.

Higher to lower concentration of which molecules in case of insulin's
diffusion?

The insulin molecule.

Quoted message said:

Quoted message said:

Quoted message said:

> > > > > Insulin resistance is occurring at the cellular level.

Quoted message said:

> > > > But still true reasonings of IR is yet un-understood fully? So other
> > > > possibilities can be thought?

Quoted message said:

> > > Actually insulin resistance is a well understood consequence of
> > > inflammation arising because of visceral adipose tissue (VAT).
> > How it interfere in insulin senstivity to target cells?

Quoted message said:

> Results in less insulin receptors and less second messenger response
> with receptor activation.
Means, VAT oriented inflammation causes lesser or down regulation of
insulin's receptors?

And possible impairment of receptor response (damaged receptors).

Will VAT oriented inflammation effect all extravascular target cells?

It typically does affect nearly all cells in the body.

May GOD bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets"
http://HeartMDPhD.com/Love/TheTruth

MD/PhD said:

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar wrote:
> Andrew, in the Holy Spirit, boldly wrote:
> > convicted neighbor Kumar wrote:
> > > Andrew, in the Holy Spirit, boldly wrote:
> > > > convicted neighbor Kumar wrote:
> > > > > Andrew, in the Holy Spirit, boldly wrote:
> > > > > > convicted neighbor Kumar wrote:

Quoted message said:

Quoted message said:

> > > > > > > Hello,

Quoted message said:

Quoted message said:

> > > > > > > "Endothelial dysfunction: a comprehensive appraisal

Quoted message said:

Quoted message said:

> > > > > > > The junction-associated actin filament system, known as FAU system, is
> > > > > > > found in the intercellular space and its contraction and relaxation
> > > > > > > controls the dimension of the intercellular space. In this way, it
> > > > > > > regulates the passage of solutes and macromolecules between the blood
> > > > > > > and the sub endothelial space. The Ca2+ concentrations, intracellular
> > > > > > > second messenger and the common factor of the external function of
> > > > > > > cells with intermittent or cyclic activities activate it, the energy
> > > > > > > is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
> > > > > > > cytokines, reactive oxygen species, thrombin, platelet activating
> > > > > > > factor, an increase of Ca2+ concentration in ischemic conditions, ATP
> > > > > > > exhaustion and other toxic substances, alter the functions of the
> > > > > > > junction-associated actin filament system and allow an opening of the
> > > > > > > intercellular space and, with that, alteration of the endothelial
> > > > > > > permeability. The FAU system is closely related to the intercellular
> > > > > > > adhesion molecules, especially with VE-cadherine maintaining a balance
> > > > > > > between adhesive and contractile forces. Both cyclic adenosine mono-
> > > > > > > phosphate (cAMP), originated through the adenylate-cyclase, and the
> > > > > > > cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
> > > > > > > guanylate-cyclase dependent pathway, are second messengers that
> > > > > > > stabilize the FAU system and counteract the induction of intercellular
> > > > > > > separation, which is done through a Ca2+-dependent calmodulin.
> > > > > > > Nitrates, behave the same way. Protein-kinase C (PKC) activation has
> > > > > > > the opposite effect (Figure 2.)

Quoted message said:

Quoted message said:

> > > > > > >http://www.cardiab.com/content/5/1/4"

Quoted message said:

Quoted message said:

> > > > > > > Above link provided detailed information on Endothelial dysfunction.

Quoted message said:

Quoted message said:

> > > > > > > Can it cause altered/abnormal movement of insulin to extravascular,
> > > > > > > transcapillary target tissues, expressing somewhat insulin resistance?

Quoted message said:

Quoted message said:

> > > > > > Increased endothelial permeability would increase rate of insulin
> > > > > > delivery to the interstitium only if the permeability had been rate-
> > > > > > limiting.

Quoted message said:

Quoted message said:

> > > > > Decreased endothelial permeability due to opposing reasons or end.
> > > > > cells swelling?

Quoted message said:

Quoted message said:

> > > > Compared to normal endothelial permeability.

Quoted message said:

Quoted message said:

> > > > > Btw, whether ionized calcium increases endothelial permeability as per
> > > > > above link?

Quoted message said:

Quoted message said:

> > > > It does.

Quoted message said:

Quoted message said:

> > > Means, diabetics who have low level of ionized calcium in their blood
> > > can have low endo. permeabilty and chances of lesser insulin movement
> > > to extravascular tissues resulting hyperglycemia?

Quoted message said:

Quoted message said:

> > Not clinically seen.

Quoted message said:

Quoted message said:

> At later stages, calcium levels decreases?

Quoted message said:

Quoted message said:

Hypocalcemia is not a characteristic of having diabetes even at later
stages.

Quoted message said:

Will lower levels of calcium not decrease endothelial permeability ?

Possibly.

Quoted message said:

If yes, it can be reason to hyperglycemia not hypoglycmia?

Reduced endothelial permeabilty has not been a clinically observed
cause of hyperglycemia.

Where it is observed? It looks quite possible?

Quoted message said:

Quoted message said:

Quoted message said:

> > Slower rates of diffusion does not necessarily mean less insulin gets
> > to target tissues.

Quoted message said:

Quoted message said:

> Insulin has short half life of just 6 minutes. It should be possible
> on altered cap.. pores dimentions?

Quoted message said:

Quoted message said:

Possible but not clinically observed.

Quoted message said:

Can you provide some links where it is studied?

As far as I know, it has not been studied.

Means, this aspect remains missed or unattended?

Quoted message said:

Clinical research starts with clinical observations.

Persisting hyperglycemia sd be clinical observation for clinical
research?

Quoted message said:

This logically follows from understanding the "scientific method."

No observations ==> no predictions ==> no experiments.

Where it is observed?

Quoted message said:

Quoted message said:

Quoted message said:

> > > > > > This would increase insulin sensitivity which is not what is observed
> > > > > > during chronic pro-inflammatory conditions of metabolic syndrome
> > > > > > (MetS) caused by the presence of visceral adipose tissue (VAT).
> > > > > Such inflammatory conditions can be meant to increase previous
> > > > > decreased endothelial permeability i.e. trying towards normal?
> > > > > > > Role of Pro-inflammatory cytokines & reactive oxygen species, which
> > > > > > > may be relating to VAT may be brainstorming in this regard as may have
> > > > > > > increasing vascular permeability, probably purpose may be to increase
> > > > > > > restricted insulin's transcapillary transport.

Quoted message said:

Quoted message said:

> > > > > > There is no transcapillary transport of insulin restricted or not.

Quoted message said:

Quoted message said:

> > > > > Why there can't be endothelial dysfunction/decreased permeability
> > > > > reason to extravascular movement of insulin which may decreases 0.2
> > > > > vascular permeability to insulin as per following reason or other
> > > > > reasonings of endo. dysfunctions as indicated on above link in detail;

Quoted message said:

Quoted message said:

> > > > > T"he junction-associated actin filament system, known as FAU system,
> > > > > is
> > > > > found in the intercellular space and its contraction and relaxation
> > > > > controls the dimension of the intercellular space. In this way, it
> > > > > regulates the passage of solutes and macromolecules between the blood
> > > > > and the sub endothelial space."

Quoted message said:

Quoted message said:

Regulation of "rates of passage (diffusion)" is not transport.

Btw, if diffusion is not a passive transport?

Diffusion is not passive transport.

It is there in http://en.wikipedia.org/wiki/Passive_transport ?

Quoted message said:

Quoted message said:

Quoted message said:

> > > You may call it insulin movement to extravascular target cells? Now
> > > pls reply previous question?

Quoted message said:

Quoted message said:

> > It is simply diffusion which is movement from higher concentration to
> > lower concentration.

Quoted message said:

Quoted message said:

> Is it of insulin's higher/lower concentration or insulin's diffusion
> is effected by others?

Quoted message said:

Quoted message said:

Diffusion is the process by which molecules disperse from higher to
lower concentration. The rate of diffusion is dependent on the size
of the molecules and their respective kinetic energies.

Quoted message said:

Higher to lower concentration of which molecules in case of insulin's
diffusion?

The insulin molecule.

Though it looks odd in view of low overall concentration of insulin,
whether such movement of insulin can also be effected by concentration
of other molecules?

Quoted message said:

Quoted message said:

Quoted message said:

> > > > > > Insulin resistance is occurring at the cellular level.

Quoted message said:

Quoted message said:

> > > > > But still true reasonings of IR is yet un-understood fully? So other
> > > > > possibilities can be thought?

Quoted message said:

Quoted message said:

> > > > Actually insulin resistance is a well understood consequence of
> > > > inflammation arising because of visceral adipose tissue (VAT).
> > > How it interfere in insulin senstivity to target cells?

Quoted message said:

Quoted message said:

> > Results in less insulin receptors and less second messenger response
> > with receptor activation.
> Means, VAT oriented inflammation causes lesser or down regulation of
> insulin's receptors?

Quoted message said:

Quoted message said:

And possible impairment of receptor response (damaged receptors).

Quoted message said:

Will VAT oriented inflammation effect all extravascular target cells?

It typically does affect nearly all cells in the body.

I may have to understand it more deeply. Thanks.

Quoted message said:

May GOD bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhDhttp://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets"http://HeartMDPhD.com/Love/TheTruth- Hide quoted text -

- Show quoted text -- Hide quoted text -

- Show quoted text -- Hide quoted text -

- Show quoted text -

On Sun, 03 Jun 2007 20:18:21 -0700, Kumar <[email hidden]>
wrote:

snip

Quoted message said:

Insulin has short half life of just 6 minutes.

snip

Kumar,
I would like to know what your source is for that info, as the
mismatch of the half-life of insulin and refined carbs is, imho, the
essential cause of type 2 diabetes.
BlackHawk

BlackHawk96 said:

On Sun, 03 Jun 2007 20:18:21 -0700, Kumar <[email hidden]>
wrote:

snip

Quoted message said:

Insulin has short half life of just 6 minutes.

snip

Kumar,
I would like to know what your source is for that info, as the
mismatch of the half-life of insulin and refined carbs is, imho, the
essential cause of type 2 diabetes.
BlackHawk

I think, it was in Textbook of Medical Physiology by Guyton& John E.
Hall. I shall recheck.

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar said:

Andrew, in the Holy Spirit, boldly wrote:
> convicted neighbor Kumar wrote:
> > Andrew, in the Holy Spirit, boldly wrote:
> > > convicted neighbor Kumar wrote:
> > > > Andrew, in the Holy Spirit, boldly wrote:
> > > > > convicted neighbor Kumar wrote:
> > > > > > Andrew, in the Holy Spirit, boldly wrote:
> > > > > > > convicted neighbor Kumar wrote:

Quoted message said:

> > > > > > > > Hello,

Quoted message said:

> > > > > > > > "Endothelial dysfunction: a comprehensive appraisal

Quoted message said:

> > > > > > > > The junction-associated actin filament system, known as FAU system, is
> > > > > > > > found in the intercellular space and its contraction and relaxation
> > > > > > > > controls the dimension of the intercellular space. In this way, it
> > > > > > > > regulates the passage of solutes and macromolecules between the blood
> > > > > > > > and the sub endothelial space. The Ca2+ concentrations, intracellular
> > > > > > > > second messenger and the common factor of the external function of
> > > > > > > > cells with intermittent or cyclic activities activate it, the energy
> > > > > > > > is provided by adenosine tri-phosphate (ATP). Pro-inflammatory
> > > > > > > > cytokines, reactive oxygen species, thrombin, platelet activating
> > > > > > > > factor, an increase of Ca2+ concentration in ischemic conditions, ATP
> > > > > > > > exhaustion and other toxic substances, alter the functions of the
> > > > > > > > junction-associated actin filament system and allow an opening of the
> > > > > > > > intercellular space and, with that, alteration of the endothelial
> > > > > > > > permeability. The FAU system is closely related to the intercellular
> > > > > > > > adhesion molecules, especially with VE-cadherine maintaining a balance
> > > > > > > > between adhesive and contractile forces. Both cyclic adenosine mono-
> > > > > > > > phosphate (cAMP), originated through the adenylate-cyclase, and the
> > > > > > > > cyclic guanine mono-phosphate (cGMP), generated by a Ca2+-nitric oxide
> > > > > > > > guanylate-cyclase dependent pathway, are second messengers that
> > > > > > > > stabilize the FAU system and counteract the induction of intercellular
> > > > > > > > separation, which is done through a Ca2+-dependent calmodulin.
> > > > > > > > Nitrates, behave the same way. Protein-kinase C (PKC) activation has
> > > > > > > > the opposite effect (Figure 2.)

Quoted message said:

> > > > > > > >http://www.cardiab.com/content/5/1/4"

Quoted message said:

> > > > > > > > Above link provided detailed information on Endothelial dysfunction.

Quoted message said:

> > > > > > > > Can it cause altered/abnormal movement of insulin to extravascular,
> > > > > > > > transcapillary target tissues, expressing somewhat insulin resistance?

Quoted message said:

> > > > > > > Increased endothelial permeability would increase rate of insulin
> > > > > > > delivery to the interstitium only if the permeability had been rate-
> > > > > > > limiting.

Quoted message said:

> > > > > > Decreased endothelial permeability due to opposing reasons or end.
> > > > > > cells swelling?

Quoted message said:

> > > > > Compared to normal endothelial permeability.

Quoted message said:

> > > > > > Btw, whether ionized calcium increases endothelial permeability as per
> > > > > > above link?

Quoted message said:

> > > > > It does.

Quoted message said:

> > > > Means, diabetics who have low level of ionized calcium in their blood
> > > > can have low endo. permeabilty and chances of lesser insulin movement
> > > > to extravascular tissues resulting hyperglycemia?

Quoted message said:

> > > Not clinically seen.

Quoted message said:

> > At later stages, calcium levels decreases?

Quoted message said:

> Hypocalcemia is not a characteristic of having diabetes even at later
> stages.

Quoted message said:

Will lower levels of calcium not decrease endothelial permeability ?

Possibly.

Quoted message said:

If yes, it can be reason to hyperglycemia not hypoglycmia?

Reduced endothelial permeabilty has not been a clinically observed
cause of hyperglycemia.

Quoted message said:

Where it is observed?

It has not been observed.

Quoted message said:

It looks quite possible?

Does not change the fact that it has not been observed.

Quoted message said:

Quoted message said:

Quoted message said:

> > > Slower rates of diffusion does not necessarily mean less insulin gets
> > > to target tissues.

Quoted message said:

> > Insulin has short half life of just 6 minutes. It should be possible
> > on altered cap.. pores dimentions?

Quoted message said:

> Possible but not clinically observed.

Quoted message said:

Can you provide some links where it is studied?

As far as I know, it has not been studied.

Quoted message said:

Means, this aspect remains missed or unattended?

No.

There are an infinite number of things that have not been studied.
This does not mean that there are an infinite number of things that
are either missed or unattended.

Quoted message said:

Quoted message said:

Clinical research starts with clinical observations.

Quoted message said:

Persisting hyperglycemia sd be clinical observation for clinical
research?

No such thing as persistent hyperglycemia for those receiving insulin
intravenously.

Quoted message said:

Quoted message said:

This logically follows from understanding the "scientific method."

No observations ==> no predictions ==> no experiments.

Quoted message said:

Where it is observed?

That which is not observed has no location.

Quoted message said:

Quoted message said:

Quoted message said:

> > > > > > > This would increase insulin sensitivity which is not what is observed
> > > > > > > during chronic pro-inflammatory conditions of metabolic syndrome
> > > > > > > (MetS) caused by the presence of visceral adipose tissue (VAT).
> > > > > > Such inflammatory conditions can be meant to increase previous
> > > > > > decreased endothelial permeability i.e. trying towards normal?
> > > > > > > > Role of Pro-inflammatory cytokines & reactive oxygen species, which
> > > > > > > > may be relating to VAT may be brainstorming in this regard as may have
> > > > > > > > increasing vascular permeability, probably purpose may be to increase
> > > > > > > > restricted insulin's transcapillary transport.

Quoted message said:

> > > > > > > There is no transcapillary transport of insulin restricted or not.

Quoted message said:

> > > > > > Why there can't be endothelial dysfunction/decreased permeability
> > > > > > reason to extravascular movement of insulin which may decreases 0.2
> > > > > > vascular permeability to insulin as per following reason or other
> > > > > > reasonings of endo. dysfunctions as indicated on above link in detail;

Quoted message said:

> > > > > > T"he junction-associated actin filament system, known as FAU system,
> > > > > > is
> > > > > > found in the intercellular space and its contraction and relaxation
> > > > > > controls the dimension of the intercellular space. In this way, it
> > > > > > regulates the passage of solutes and macromolecules between the blood
> > > > > > and the sub endothelial space."

Quoted message said:

> Regulation of "rates of passage (diffusion)" is not transport.
Btw, if diffusion is not a passive transport?

Diffusion is not passive transport.

It is there in http://en.wikipedia.org/wiki/Passive_transport ?

When there is no transporter, there is no transport.

The wiki entry you cite is erroneous about diffusion being passive
transport.

Quoted message said:

Quoted message said:

Quoted message said:

> > > > You may call it insulin movement to extravascular target cells? Now
> > > > pls reply previous question?

Quoted message said:

> > > It is simply diffusion which is movement from higher concentration to
> > > lower concentration.

Quoted message said:

> > Is it of insulin's higher/lower concentration or insulin's diffusion
> > is effected by others?

Quoted message said:

> Diffusion is the process by which molecules disperse from higher to
> lower concentration. The rate of diffusion is dependent on the size
> of the molecules and their respective kinetic energies.

Quoted message said:

Higher to lower concentration of which molecules in case of insulin's
diffusion?

The insulin molecule.

Quoted message said:

Though it looks odd in view of low overall concentration of insulin,
whether such movement of insulin can also be effected by concentration
of other molecules?

Diffusion of insulin is not affected by the concentration of other
molecules.

Quoted message said:

Quoted message said:

Quoted message said:

> > > > > > > Insulin resistance is occurring at the cellular level.

Quoted message said:

> > > > > > But still true reasonings of IR is yet un-understood fully? So other
> > > > > > possibilities can be thought?

Quoted message said:

> > > > > Actually insulin resistance is a well understood consequence of
> > > > > inflammation arising because of visceral adipose tissue (VAT).
> > > > How it interfere in insulin senstivity to target cells?

Quoted message said:

> > > Results in less insulin receptors and less second messenger response
> > > with receptor activation.
> > Means, VAT oriented inflammation causes lesser or down regulation of
> > insulin's receptors?

Quoted message said:

> And possible impairment of receptor response (damaged receptors).

Quoted message said:

Will VAT oriented inflammation effect all extravascular target cells?

It typically does affect nearly all cells in the body.

Quoted message said:

I may have to understand it more deeply. Thanks.

Thanks be to GOD.

May HE bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."
http://HeartMDPhD.com/Love/TheTruth

MD/PhD said:

convicted neighbor Kumar said:

Andrew, in the Holy Spirit, boldly wrote:

Quoted message said:

Quoted message said:

Reduced endothelial permeabilty has not been a clinically observed
cause of hyperglycemia.

Where it is observed?

It has not been observed.

I could not find any study to it. Is it yet studied?

Quoted message said:

Quoted message said:

It looks quite possible?

Does not change the fact that it has not been observed.

Quoted message said:

Quoted message said:

> > > > Slower rates of diffusion does not necessarily mean less insulin gets
> > > > to target tissues.

Quoted message said:

Quoted message said:

> > > Insulin has short half life of just 6 minutes. It should be possible
> > > on altered cap.. pores dimentions?

Quoted message said:

Quoted message said:

> > Possible but not clinically observed.

Quoted message said:

Quoted message said:

> Can you provide some links where it is studied?

Quoted message said:

Quoted message said:

As far as I know, it has not been studied.

Means, this aspect remains missed or unattended?

No.

There are an infinite number of things that have not been studied.
This does not mean that there are an infinite number of things that
are either missed or unattended.

Quoted message said:

Quoted message said:

Clinical research starts with clinical observations.

Persisting hyperglycemia sd be clinical observation for clinical
research?

No such thing as persistent hyperglycemia for those receiving insulin
intravenously.

That can be due to addition of more insulin. At decreased
extravascular movement, control of glucose levels are still possible
by additional insulin?

Quoted message said:

Quoted message said:

Quoted message said:

This logically follows from understanding the "scientific method."

Quoted message said:

Quoted message said:

No observations ==> no predictions ==> no experiments.

Where it is observed?

That which is not observed has no location.

True reasoning to IR is still unclear.Many possibilities are thought:-

http://google.diabetes.org/search?q=insulin+resistance&ie=UTF-8&site=default_collection&access=p&output=xml_no_dtd&client=default_frontend&proxystylesheet=new_google_template&proxyreload=1&Search.x=13&Search.y=4

Quoted message said:

snip> > > > > And possible impairment of receptor response (damaged
receptors).

Quoted message said:

Quoted message said:

Quoted message said:

> Will VAT oriented inflammation effect all extravascular target cells?

Quoted message said:

Quoted message said:

It typically does affect nearly all cells in the body.

I may have to understand it more deeply. Thanks.

Thanks be to GOD.

May HE bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhDhttp://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."http://HeartMDPhD.com/Love/TheTruth- Hide quoted text -

- Show quoted text -- Hide quoted text -

- Show quoted text -- Hide quoted text -

- Show quoted text -- Hide quoted text -

- Show quoted text -

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar said:

Andrew, in the Holy Spirit, boldly wrote:

Quoted message said:

> Reduced endothelial permeabilty has not been a clinically observed
> cause of hyperglycemia.
Where it is observed?

It has not been observed.

I could not find any study to it.

Can't study what one does not observe.

Quoted message said:

Is it yet studied?

Until it is observed, it will not be studied.

Quoted message said:

Quoted message said:

Quoted message said:

It looks quite possible?

Does not change the fact that it has not been observed.

Quoted message said:

> > > > > Slower rates of diffusion does not necessarily mean less insulin gets
> > > > > to target tissues.

Quoted message said:

> > > > Insulin has short half life of just 6 minutes. It should be possible
> > > > on altered cap.. pores dimentions?

Quoted message said:

> > > Possible but not clinically observed.

Quoted message said:

> > Can you provide some links where it is studied?

Quoted message said:

> As far as I know, it has not been studied.
Means, this aspect remains missed or unattended?

No.

There are an infinite number of things that have not been studied.
This does not mean that there are an infinite number of things that
are either missed or unattended.

Quoted message said:

> Clinical research starts with clinical observations.
Persisting hyperglycemia sd be clinical observation for clinical
research?

No such thing as persistent hyperglycemia for those receiving insulin
intravenously.

That can be due to addition of more insulin. At decreased
extravascular movement, control of glucose levels are still possible
by additional insulin?

Then it would not be persistent hyperglycemia.

Quoted message said:

Quoted message said:

Quoted message said:

> This logically follows from understanding the "scientific method."

Quoted message said:

> No observations ==> no predictions ==> no experiments.
Where it is observed?

That which is not observed has no location.

True reasoning to IR is still unclear.Many possibilities are thought:-

http://google.diabetes.org/search?q=insulin+resistance&ie=UTF-8&site=default_collection&access=p&output=xml_no_dtd&client=default_frontend&proxystylesheet=new_google_template&proxyreload=1&Search.x=13&Search.y=4

The pathophysiology of IR is clearly arising from inflammation.

May GOD bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."
http://HeartMDPhD.com/Love/TheTruth

MD/PhD said:

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar wrote:
> Andrew, in the Holy Spirit, boldly wrote:

Quoted message said:

Quoted message said:

> > Reduced endothelial permeabilty has not been a clinically observed
> > cause of hyperglycemia.
> Where it is observed?

Quoted message said:

Quoted message said:

It has not been observed.

Quoted message said:

I could not find any study to it.

Can't study what one does not observe.

Quoted message said:

Is it yet studied?

Until it is observed, it will not be studied.

How it can be observed? So interpreted IR may be expressed either of--
decreased movement or decreased senstiveness or insufficient
secretion. How it can be justified and observed, hyperglycemia is
either of these?

Quoted message said:

Quoted message said:

Quoted message said:

> It looks quite possible?

Quoted message said:

Quoted message said:

Does not change the fact that it has not been observed.

Quoted message said:

Quoted message said:

> > > > > > Slower rates of diffusion does not necessarily mean less insulin gets
> > > > > > to target tissues.

Quoted message said:

Quoted message said:

> > > > > Insulin has short half life of just 6 minutes. It should be possible
> > > > > on altered cap.. pores dimentions?

Quoted message said:

Quoted message said:

> > > > Possible but not clinically observed.

Quoted message said:

Quoted message said:

> > > Can you provide some links where it is studied?

Quoted message said:

Quoted message said:

> > As far as I know, it has not been studied.
> Means, this aspect remains missed or unattended?

Quoted message said:

Quoted message said:

No.

Quoted message said:

Quoted message said:

There are an infinite number of things that have not been studied.
This does not mean that there are an infinite number of things that
are either missed or unattended.

Quoted message said:

Quoted message said:

> > Clinical research starts with clinical observations.
> Persisting hyperglycemia sd be clinical observation for clinical
> research?

Quoted message said:

Quoted message said:

No such thing as persistent hyperglycemia for those receiving insulin
intravenously.

Quoted message said:

That can be due to addition of more insulin. At decreased
extravascular movement, control of glucose levels are still possible
by additional insulin?

Then it would not be persistent hyperglycemia.

I mentioned for "no such thing as persistent hyperglycemia..".
Decreased endogenous insulin movement can be compensated by added
insulin, resulting control. I mentioned decreased movement not no
movement.

Quoted message said:

Quoted message said:

Quoted message said:

> > This logically follows from understanding the "scientific method."

Quoted message said:

Quoted message said:

> > No observations ==> no predictions ==> no experiments.
> Where it is observed?

Quoted message said:

Quoted message said:

That which is not observed has no location.

Quoted message said:

True reasoning to IR is still unclear.Many possibilities are thought:-

Quoted message said:

http://google.diabetes.org/search?q=insulin+resistance&ie=UTF-8&site=...

The pathophysiology of IR is clearly arising from inflammation.

I shall try to give you ADA link later.

Quoted message said:

May GOD bless you in HIS mighty way making you hungrier than ever.

Thanks. Till I am actual impaired insulin production, I have no issue
on manipulating optimal food intake for control. Though I am now
trying but inabilty to practice such manipulation can only be the
disease.

Quoted message said:

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhDhttp://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets."http://HeartMDPhD.com/Love/TheTruth- Hide quoted text -

- Show quoted text -

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar said:

Andrew, in the Holy Spirit, boldly wrote:
> convicted neighbor Kumar wrote:
> > Andrew, in the Holy Spirit, boldly wrote:

Quoted message said:

> > > Reduced endothelial permeabilty has not been a clinically observed
> > > cause of hyperglycemia.
> > Where it is observed?

Quoted message said:

> It has not been observed.

Quoted message said:

I could not find any study to it.

Can't study what one does not observe.

Quoted message said:

Is it yet studied?

Until it is observed, it will not be studied.

How it can be observed?

By happening.

Quoted message said:

So interpreted IR may be expressed either of--
decreased movement or decreased senstiveness or insufficient
secretion. How it can be justified and observed, hyperglycemia is
either of these?

When the cells of a hyperglycemic person respond to insulin normally
in vitro (outside the body) and the person is not a type-1 diabetic.

Quoted message said:

Quoted message said:

Quoted message said:

> > It looks quite possible?

Quoted message said:

> Does not change the fact that it has not been observed.

Quoted message said:

> > > > > > > Slower rates of diffusion does not necessarily mean less insulin gets
> > > > > > > to target tissues.

Quoted message said:

> > > > > > Insulin has short half life of just 6 minutes. It should be possible
> > > > > > on altered cap.. pores dimentions?

Quoted message said:

> > > > > Possible but not clinically observed.

Quoted message said:

> > > > Can you provide some links where it is studied?

Quoted message said:

> > > As far as I know, it has not been studied.
> > Means, this aspect remains missed or unattended?

Quoted message said:

> No.

Quoted message said:

> There are an infinite number of things that have not been studied.
> This does not mean that there are an infinite number of things that
> are either missed or unattended.

Quoted message said:

> > > Clinical research starts with clinical observations.
> > Persisting hyperglycemia sd be clinical observation for clinical
> > research?

Quoted message said:

> No such thing as persistent hyperglycemia for those receiving insulin
> intravenously.

Quoted message said:

That can be due to addition of more insulin. At decreased
extravascular movement, control of glucose levels are still possible
by additional insulin?

Then it would not be persistent hyperglycemia.

I mentioned for "no such thing as persistent hyperglycemia..".
Decreased endogenous insulin movement can be compensated by added
insulin, resulting control. I mentioned decreased movement not no
movement.

The behavior would not be the same. In the extreme case of decreased
insulin permeabilty (ie impermeable), no amount of insulin would
overcome the problem and then truly persistent hyperglycemia would
occur.

Quoted message said:

Quoted message said:

Quoted message said:

> > > This logically follows from understanding the "scientific method."

Quoted message said:

> > > No observations ==> no predictions ==> no experiments.
> > Where it is observed?

Quoted message said:

> That which is not observed has no location.

Quoted message said:

True reasoning to IR is still unclear.Many possibilities are thought:-

Quoted message said:

http://google.diabetes.org/search?q=insulin+resistance&ie=UTF-8&site=...

The pathophysiology of IR is clearly arising from inflammation.

I shall try to give you ADA link later.

That would simply show that someone does not have a clear
understanding of the pathophysiology of IR.

Quoted message said:

Quoted message said:

May GOD bless you in HIS mighty way making you hungrier than ever.

Thanks. Till I am actual impaired insulin production, I have no issue
on manipulating optimal food intake for control. Though I am now
trying but inabilty to practice such manipulation can only be the
disease.

No. Your inability to eat less down to the optimal amount is arising
from satan's lie that "hunger is bad" residing in your heart.

You will remain in my prayers, dear neighbor Kumar whom I love
unconditionally.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets"
http://HeartMDPhD.com/Love/TheTruth

MD/PhD said:

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar wrote:
> Andrew, in the Holy Spirit, boldly wrote:
> > convicted neighbor Kumar wrote:
> > > Andrew, in the Holy Spirit, boldly wrote:

Quoted message said:

Quoted message said:

> > > > Reduced endothelial permeabilty has not been a clinically observed
> > > > cause of hyperglycemia.
> > > Where it is observed?

Quoted message said:

Quoted message said:

> > It has not been observed.

Quoted message said:

Quoted message said:

> I could not find any study to it.

Quoted message said:

Quoted message said:

Can't study what one does not observe.

Quoted message said:

Quoted message said:

> Is it yet studied?

Quoted message said:

Quoted message said:

Until it is observed, it will not be studied.

Quoted message said:

How it can be observed?

By happening.

Happening is hyperglycemia. Probably, dawn regulation of receptors may
be a normal physiology for a purpose to avoid excess glucose intake
and initiate its store?

Quoted message said:

Quoted message said:

So interpreted IR may be expressed either of--
decreased movement or decreased senstiveness or insufficient
secretion. How it can be justified and observed, hyperglycemia is
either of these?

When the cells of a hyperglycemic person respond to insulin normally
in vitro (outside the body) and the person is not a type-1 diabetic.

Don't they respond alike it?

If they, it can indicate no insentivity of insulin?

Quoted message said:

Quoted message said:

Quoted message said:

> > > It looks quite possible?

Quoted message said:

Quoted message said:

> > Does not change the fact that it has not been observed.

Quoted message said:

Quoted message said:

> > > > > > > > Slower rates of diffusion does not necessarily mean less insulin gets
> > > > > > > > to target tissues.

Quoted message said:

Quoted message said:

> > > > > > > Insulin has short half life of just 6 minutes. It should be possible
> > > > > > > on altered cap.. pores dimentions?

Quoted message said:

Quoted message said:

> > > > > > Possible but not clinically observed.

Quoted message said:

Quoted message said:

> > > > > Can you provide some links where it is studied?

Quoted message said:

Quoted message said:

> > > > As far as I know, it has not been studied.
> > > Means, this aspect remains missed or unattended?

Quoted message said:

Quoted message said:

> > No.

Quoted message said:

Quoted message said:

> > There are an infinite number of things that have not been studied.
> > This does not mean that there are an infinite number of things that
> > are either missed or unattended.

Quoted message said:

Quoted message said:

> > > > Clinical research starts with clinical observations.
> > > Persisting hyperglycemia sd be clinical observation for clinical
> > > research?

Quoted message said:

Quoted message said:

> > No such thing as persistent hyperglycemia for those receiving insulin
> > intravenously.

Quoted message said:

Quoted message said:

> That can be due to addition of more insulin. At decreased
> extravascular movement, control of glucose levels are still possible
> by additional insulin?

Quoted message said:

Quoted message said:

Then it would not be persistent hyperglycemia.

Quoted message said:

I mentioned for "no such thing as persistent hyperglycemia..".
Decreased endogenous insulin movement can be compensated by added
insulin, resulting control. I mentioned decreased movement not no
movement.

The behavior would not be the same. In the extreme case of decreased
insulin permeabilty (ie impermeable), no amount of insulin would
overcome the problem and then truly persistent hyperglycemia would
occur.

There can also be sub extreme cases?

Quoted message said:

Quoted message said:

Quoted message said:

> > > > This logically follows from understanding the "scientific method."

Quoted message said:

Quoted message said:

> > > > No observations ==> no predictions ==> no experiments.
> > > Where it is observed?

Quoted message said:

Quoted message said:

> > That which is not observed has no location.

Quoted message said:

Quoted message said:

> True reasoning to IR is still unclear.Many possibilities are thought:-

Quoted message said:

Quoted message said:

>http://google.diabetes.org/search?q=insulin+resistance&ie=UTF-8&site=...

Quoted message said:

Quoted message said:

The pathophysiology of IR is clearly arising from inflammation.

Quoted message said:

I shall try to give you ADA link later.

That would simply show that someone does not have a clear
understanding of the pathophysiology of IR.

Yes. so other aspects can be possible.

Quoted message said:

Quoted message said:

Quoted message said:

May GOD bless you in HIS mighty way making you hungrier than ever.

Quoted message said:

Thanks. Till I am actual impaired insulin production, I have no issue
on manipulating optimal food intake for control. Though I am now
trying but inabilty to practice such manipulation can only be the
disease.

No. Your inability to eat less down to the optimal amount is arising
from satan's lie that "hunger is bad" residing in your heart.

You will remain in my prayers, dear neighbor Kumar whom I love
unconditionally.

Thanks.

Quoted message said:

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhDhttp://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets"http://HeartMDPhD.com/Love/TheTruth- Hide quoted text -

- Show quoted text -- Hide quoted text -

- Show quoted text -

convicted neighbor Kumar said:

Andrew said:

convicted neighbor Kumar said:

Andrew, in the Holy Spirit, boldly wrote:
> convicted neighbor Kumar wrote:
> > Andrew, in the Holy Spirit, boldly wrote:
> > > convicted neighbor Kumar wrote:
> > > > Andrew, in the Holy Spirit, boldly wrote:

Quoted message said:

> > > > > Reduced endothelial permeabilty has not been a clinically observed
> > > > > cause of hyperglycemia.

Quoted message said:

Quoted message said:

> > > > Where it is observed?

Quoted message said:

> > > It has not been observed.

Quoted message said:

> > I could not find any study to it.

Quoted message said:

> Can't study what one does not observe.

Quoted message said:

> > Is it yet studied?

Quoted message said:

> Until it is observed, it will not be studied.

Quoted message said:

How it can be observed?

By happening.

Happening is hyperglycemia.

.... that responds to insulin.

Quoted message said:

Probably, dawn regulation of receptors may
be a normal physiology for a purpose to avoid excess glucose intake
and initiate its store?

Down-regulation of insulin receptors is pathological.

Quoted message said:

Quoted message said:

Quoted message said:

So interpreted IR may be expressed either of--
decreased movement or decreased senstiveness or insufficient
secretion. How it can be justified and observed, hyperglycemia is
either of these?

When the cells of a hyperglycemic person respond to insulin normally
in vitro (outside the body) and the person is not a type-1 diabetic.

Don't they respond alike it?

The cells of a type-2 diabetic are resistant to insulin in vitro.

Quoted message said:

If they, it can indicate no insentivity of insulin?

Such is the case for normals and type-1 diabetics but not type-2.

Quoted message said:

Quoted message said:

Quoted message said:

> > > > It looks quite possible?

Quoted message said:

> > > Does not change the fact that it has not been observed.

Quoted message said:

> > > > > > > > > Slower rates of diffusion does not necessarily mean less insulin gets
> > > > > > > > > to target tissues.

Quoted message said:

> > > > > > > > Insulin has short half life of just 6 minutes. It should be possible
> > > > > > > > on altered cap.. pores dimentions?

Quoted message said:

> > > > > > > Possible but not clinically observed.

Quoted message said:

> > > > > > Can you provide some links where it is studied?

Quoted message said:

> > > > > As far as I know, it has not been studied.
> > > > Means, this aspect remains missed or unattended?

Quoted message said:

> > > No.

Quoted message said:

> > > There are an infinite number of things that have not been studied.
> > > This does not mean that there are an infinite number of things that
> > > are either missed or unattended.

Quoted message said:

> > > > > Clinical research starts with clinical observations.
> > > > Persisting hyperglycemia sd be clinical observation for clinical
> > > > research?

Quoted message said:

> > > No such thing as persistent hyperglycemia for those receiving insulin
> > > intravenously.

Quoted message said:

> > That can be due to addition of more insulin. At decreased
> > extravascular movement, control of glucose levels are still possible
> > by additional insulin?

Quoted message said:

> Then it would not be persistent hyperglycemia.

Quoted message said:

I mentioned for "no such thing as persistent hyperglycemia..".
Decreased endogenous insulin movement can be compensated by added
insulin, resulting control. I mentioned decreased movement not no
movement.

The behavior would not be the same. In the extreme case of decreased
insulin permeabilty (ie impermeable), no amount of insulin would
overcome the problem and then truly persistent hyperglycemia would
occur.

There can also be sub extreme cases?

They would have kinetics that approach the extreme case.

Quoted message said:

Quoted message said:

Quoted message said:

> > > > > This logically follows from understanding the "scientific method."

Quoted message said:

> > > > > No observations ==> no predictions ==> no experiments.
> > > > Where it is observed?

Quoted message said:

> > > That which is not observed has no location.

Quoted message said:

> > True reasoning to IR is still unclear.Many possibilities are thought:-

Quoted message said:

> >http://google.diabetes.org/search?q=insulin+resistance&ie=UTF-8&site=...

Quoted message said:

> The pathophysiology of IR is clearly arising from inflammation.

Quoted message said:

I shall try to give you ADA link later.

That would simply show that someone does not have a clear
understanding of the pathophysiology of IR.

Yes. so other aspects can be possible.

Pathophysiology is not an aspect or perspective.

Quoted message said:

Quoted message said:

Quoted message said:

> May GOD bless you in HIS mighty way making you hungrier than ever.

Quoted message said:

Thanks. Till I am actual impaired insulin production, I have no issue
on manipulating optimal food intake for control. Though I am now
trying but inabilty to practice such manipulation can only be the
disease.

No. Your inability to eat less down to the optimal amount is arising
from satan's lie that "hunger is bad" residing in your heart.

You will remain in my prayers, dear neighbor Kumar whom I love
unconditionally.

Thanks.

Thanks be to GOD.

May GOD bless you in HIS mighty way making you hungrier than ever.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

"Unlike the 2PD-OMER Approach, weight loss diets can't be combined
with well-balanced diets"
http://HeartMDPhD.com/Love/TheTruth