Insulin Resistance/Fats related? 
Author Message
 Insulin Resistance/Fats related?

Hello,

"Insulin
When you eat a candy bar or a meal, the presence of glucose, amino
acids or fatty acids in the intestine stimulates the pancreas to
secrete a hormone called insulin. Insulin acts on many cells in your
body, especially those in the liver, muscle and fat tissue. Insulin
tells the cells to do the following:
Absorb glucose, fatty acids and amino acids
Stop breaking down:
glucose, fatty acids and amino acids
glycogen into glucose
fats into fatty acids and glycerol
proteins into amino acids
Start building:
glycogen from glucose
fats (triglycerides) from glycerol and fatty acids
proteins from amino acids

How Fat is Stored in Your Body

Chylomicrons do not last long in the {*filter*}stream -- only about eight
minutes -- because enzymes called lipoprotein lipases break the fats
into fatty acids. Lipoprotein lipases are found in the walls of {*filter*}
vessels in fat tissue, muscle tissue and heart muscle. The activity of
lipoprotein lipases depends upon the levels of insulin in the body. If
insulin is high, then the lipases are highly active; if insulin is low,
the lipases are inactive.The fatty acids are then absorbed from the
{*filter*} into fat cells, muscle cells and liver cells. In these cells,
under stimulation by insulin, fatty acids are made into fat molecules
and stored as fat droplets.It is also possible for fat cells to take up
glucose and amino acids, which have been absorbed into the {*filter*}stream
after a meal, and convert those into fat molecules....Given a choice, a
fat cell will grab the fat and store it rather than the carbohydrates
because fat is so much easier to store.

  http://www.***.com/ ;

In a normal person, a small amount of insulin is produced after eating
("postprandial"), and it signals the body to absorb the sugars from the
cooking.net">food at a steady rate. In an "insulin resistant" person the message
does not get to the cells so the sugar remains in the {*filter*} for long
periods of time while ever more insulin is released in an attempt to
trigger the sugar-uptake. The sugar circulates in the {*filter*} for several
hours and then is taken into the cells very rapidly, leading to a steep
drop in {*filter*} sugar and a hypoglycaemic reaction several hours after
the meal.

At a later stage, frank hyperglycemia develops as pancreatic ?-cells
are unable to produce adequate insulin to maintain normal {*filter*} sugar
levels ("euglycemia").

Various disease states make the body tissues more resistant to the
actions of insulin. Example include infection (TNFa) and acidosis.
Recent research involves the relative roles of adipokines (the
cytokines produced by adipose tissue) in modifying insulin resistance.
Insulin resistance and atherosclerosis often appear together.
http://www.***.com/ ;

In consideration of above quotes, I have following questions:-

1. Can insulin resistance be treated as an inflamatory disease?

2. Can't glucose conversion into fats also happen in other cells than
fat cells?

3. Whether more insulin--natural or medicated can promote more fat
store into cells which may ultimate result into insulin resistance?

4. Whether insulin is required for entry of glucose into fat(not muscle
cells) cells?

5. Whether elevated glucose level is needed to correct inflammatory
conditions?

6. Whether immune cells or their multiplications or inflammatory
responses, need glucose as energy source in case of any
inflammation/infection and whether insulin is needed for pursuing such
responces?

Best wishes.



Sat, 19 Jul 2008 17:30:58 GMT
 Insulin Resistance/Fats related?
The extra insulin contributes to the "poisoning" of liver and muscle cells
by fat. The fat then makes the cells insulin resistant even in the absence
of excess cortisol. Russ Farris    http://www.potbellysyndrome.com
==================

Hello,

3. Whether more insulin--natural or medicated can promote more fat
store into cells which may ultimate result into insulin resistance?

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Sun, 20 Jul 2008 01:49:08 GMT
 Insulin Resistance/Fats related?
Yes, insulin is required to push glucose into fat cells. Fat cells never
become insulin resistant; that's why insulin resistant people become fat
sooner or later. Russ Farris    http://www.potbellysyndrome.com
=============

Hello,

4. Whether insulin is required for entry of glucose into fat(not muscle
cells) cells?

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Sun, 20 Jul 2008 01:52:25 GMT
 Insulin Resistance/Fats related?
Hi Kumar. I think you would get better answers to your questions if you made
your posts a lot shorter and focused each one on just one thing. It is hard
to answer your questions the way you put them, but I will take a stab at it.
        Insulin resistance is caused initially by cortisol's
counterregulation of insulin. During counterregulation, liver and muscle
cells burn more fat and less glucose, and over a period of years this
"poisons" the liver and muscle cells with fat. The "poisoned" cells become
insulin resistant, then, even when no cortisol is present.
        Most of the excess cortisol is triggered by inflammation from
chronic infections, so it is correct, in one sense, to say that insulin
resistance is an inflammatory disease.
        Also, you would be taken more seriously if you stopped
cross-posting. Russ Farris    http://www.potbellysyndrome.com


1. Can insulin resistance be treated as an inflamatory disease?

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Sun, 20 Jul 2008 01:45:32 GMT
 Insulin Resistance/Fats related?
Hello Russell Farris,

Thanks for reply, good link and advice about cross posting.

Cortisol's counterregulation of insulin is a new concept to me.

Can this happen;

First glucose is used by muscle cells. If still excess glucose is
available it is absorbed into fat cells for its conversion into fats.
It is not sure to me whether fat cells also resist such excess glucose
into them. Probably after it, still excess glucose may be converted
into protiens. Can't inflammatory cytokines produced by fat cells
triggering insulin resistance be meant to resist more glucose into fat
cells if sufficient fats are already stored?

Best regards.

Quote:

> Hi Kumar. I think you would get better answers to your questions if you made
> your posts a lot shorter and focused each one on just one thing. It is hard
> to answer your questions the way you put them, but I will take a stab at it.
>         Insulin resistance is caused initially by cortisol's
> counterregulation of insulin. During counterregulation, liver and muscle
> cells burn more fat and less glucose, and over a period of years this
> "poisons" the liver and muscle cells with fat. The "poisoned" cells become
> insulin resistant, then, even when no cortisol is present.
>         Most of the excess cortisol is triggered by inflammation from
> chronic infections, so it is correct, in one sense, to say that insulin
> resistance is an inflammatory disease.
>         Also, you would be taken more seriously if you stopped
> cross-posting. Russ Farris    http://www.potbellysyndrome.com



> 1. Can insulin resistance be treated as an inflamatory disease?

> ----== Posted via Newsfeeds.Com - Unlimited-Unrestricted-Secure Usenet News==----
> http://www.newsfeeds.com The #1 Newsgroup Service in the World! 120,000+ Newsgroups
> ----= East and West-Coast Server Farms - Total Privacy via Encryption =----



Sun, 20 Jul 2008 02:25:15 GMT
 Insulin Resistance/Fats related?
Hi Kumar. It appears that fat cells continue to absorb glucose, and produce
fat, as long as glucose and insulin are both present. I'm not sure how the
recently-discovered, fat-cell produced inflammatory cytokines fit into this
picture. Russ Farris    http://www.potbellysyndrome.com


Quote:
> Can this happen;
> First glucose is used by muscle cells. If still excess glucose is
> available it is absorbed into fat cells for its conversion into fats.
> It is not sure to me whether fat cells also resist such excess glucose
> into them. Probably after it, still excess glucose may be converted
> into protiens. Can't inflammatory cytokines produced by fat cells
> triggering insulin resistance be meant to resist more glucose into fat
> cells if sufficient fats are already stored?

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Sun, 20 Jul 2008 12:57:49 GMT
 Insulin Resistance/Fats related?
Hi Farris,

I am also not clear on this issue but there can be some resistance to
unlimited store of fats in fat cells--esp. visceral. Either they resist
by producing inflammatory cytokines  or leak which may encourage immune
responses.

Btw, why insulin resistant people get greater visceral adiposity(pot
belly) instead of or in addition to subcutaneous adiposity? Whether
production of inflammatory cytokines are more related to  visceral fat
cells than to subcutaneous fat cells?

Quote:

> Hi Kumar. It appears that fat cells continue to absorb glucose, and produce
> fat, as long as glucose and insulin are both present. I'm not sure how the
> recently-discovered, fat-cell produced inflammatory cytokines fit into this
> picture. Russ Farris    http://www.potbellysyndrome.com



> > Can this happen;
> > First glucose is used by muscle cells. If still excess glucose is
> > available it is absorbed into fat cells for its conversion into fats.
> > It is not sure to me whether fat cells also resist such excess glucose
> > into them. Probably after it, still excess glucose may be converted
> > into protiens. Can't inflammatory cytokines produced by fat cells
> > triggering insulin resistance be meant to resist more glucose into fat
> > cells if sufficient fats are already stored?

> ----== Posted via Newsfeeds.Com - Unlimited-Unrestricted-Secure Usenet News==----
> http://www.newsfeeds.com The #1 Newsgroup Service in the World! 120,000+ Newsgroups
> ----= East and West-Coast Server Farms - Total Privacy via Encryption =----



Sun, 20 Jul 2008 14:24:12 GMT
 Insulin Resistance/Fats related?
"Various disease states make the body tissues more resistant to the
actions of insulin. Example include infection (TNFa) and acidosis.
Recent research involves the relative roles of adipokines (the
cytokines produced by adipose tissue) in modifying insulin resistance.

Causes of insulin resistance
Obesity
Haemochromatosis
Polycystic ovarian syndrome (PCOS)
Hypercortisolism (e.g. steroid use or Cushing's disease)
{*filter*} (e.g. rifampicin, isoniazid, olanzapine, risperidone,
progestogens, many antiretrovirals, possibly {*filter*})
Genes
http://www.***.com/ ;

Whether above quote tells all possible causes for getting insulin
resistance or not? If not, what are other possibilities?



Mon, 21 Jul 2008 00:11:48 GMT
 
 [ 8 post ] 

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