Re: Increasing insulin sensitivity with drugs maybe NOT a good idea?


The concept of insulin sensitivity and insulin resistance has confused
me. The explanation do not always seem to fit what I have observed.
I read all about the clamp procedures and on and on.

Exercise seems to reduce the glucose level in my case. In fact
they result in many 911 runs. I assume it is my ignorance that
I cannot see a lot of the claims

My recent personal experiences raises a lot of questions since
the control of a long term parasite infection has altered my
insulin requirements a lot.

I will say I am pissed to the core over some docs that assumed so
much. They took the gross money and I suffered.


On Thu, 4 Oct 2007 08:56:59 -0400, "rk" <rksays@xxxxxxxx> wrote:

thanks for the info gys. but what exactly is " Heat shock proteins"?
is it adding something to your diet? or what? it's kinda early here
for me and I just woke up, so after I read it again a bit later I might
figure it out.. but in the meantime, for others would you be so kind
to further explain it? I'm interested in it because of it mentioning its
potential for preventing or treating neurodegenerative disorders,
(which I have) controlling inflammation, and possibly even slowing
the aging process (which aren't we all interested in :))

thanks

rk, t1



"GysdeJongh" <jongh711@xxxxxxxxx> wrote in message
news:4704e037$0$25501$ba620dc5@xxxxxxxxxxxxxxxxxxxxxx
| "Susan" <nevermind@xxxxxxxxxx> wrote in message
| news:5miqaqFdpkotU1@xxxxxxxxxxxxxxxxxxxxx
| > bigvince wrote:
| >> Maybe exercise does improve insulin resistance
|
| > No, Vince, studies of actual receptor sensitivity have not borne that
out,
| > but exercise has many other benefits for a DM, including burning off
| > glucose and increasing muscle mass for more glucose disposal.
| >
| > What you've cited here is merely speculative, not a measurement at
all.
|
| Hi Susan,
| this can become a semantic discussion of course :(
|
| There are many benefits of exercise.Exercise , moving your muscles , has
a
| lot of efects.Than there is the acedemic discussion if the insulin
receptor
| ITSELF is involved in those exercise benefits.
|
| It is :)
| Just one of the effects works like this :
| 1) If you have too much fat in your muscles then diacyl glycerol is
formed
| by metabolising the fat
| 2)Diacyl glycerol will upregulate a special type of protein kinase
| 3)This , wrong type , of protein kinase will phosphorilate the insulin
| receptor at the wrong place which will render the insulin receptor
inactive
| 4) If you exercise you will lose the fat in your muscles , which will
| restore the sensitivity of the insulin receptor
|
| Again , this is just one effect of exercise
| Again this is just one way the insulin sensitivity is restored by
exercise
|
| Here are a few articles for just this one effect :
| (I posted the effects of ATPK just a few days ago , with a free review :
| "AMPK a therapeutic target for type 2 diabetes" ) :
|
| Am J Clin Nutr. 2007 Mar;85(3):662-77.
| Skeletal muscle lipid deposition and insulin resistance: effect of
dietary
| fatty acids and exercise.
|
| Mounting evidence indicates that elevated intramyocellular
triacylglycerol
| concentrations are associated with diminished insulin sensitivity in
| skeletal muscle. This lipid accumulation is most likely due to enhanced
| fatty acid uptake into the muscle coupled with diminished mitochondrial
| lipid oxidation. The excess fatty acids are esterified and either stored
or
| metabolized to various molecules that may participate or interfere with
| normal cellular signaling, particularly insulin-mediated signal
| transduction, thus altering cellular and, subsequently, whole-body
glucose
| metabolism. Impaired insulin responsiveness, if not managed, can further
| progress to type 2 diabetes mellitus, an all too common condition. For
most
| of the human population this is avoidable, given that causes of
| intramyocellular lipid deposition are predominantly lifestyle-mediated.
| Chronic overconsumption of calories coupled with deleterious intakes of
| saturated or trans-unsaturated fatty acids inconsistent with the
| recommendations outlined in the Dietary Guidelines for Americans have
been
| shown to increase the risk of insulin resistance. Furthermore, lack of
| exercise, which can have a profound effect on skeletal muscle lipid
| turnover, is implicated in this lipid-induced insulin resistance. This
| review summarizes the current understanding of the effects of elevated
| intramyocellular lipids on insulin signaling and how these effects may
be
| altered by varying dietary fat composition and exercise.
|
| PMID: 17344486
|
|
| Pathways mediating fat-induced insulin resistance
| The insulin resistance associated with obesity and habitual consumption
of
| fatty diets has been linked to increased intromyocellular levels of
stored
| triglycerides and fatty acid derivatives. At least in subjects who are
not
| engaged in aerobic training, insulin resistance correlates well with the
| quantity of triglyceride stored in muscle fibers [1-5], and there is
good
| reason to suspect that certain fatty acid-derived compounds are
mediators of
| this insulin resistance. In particular, diacylglycerol, synthesized de
novo
| from increased levels of fatty acyl-coA, has been shown to activate
certain
| classic and novel isoforms of protein kinase C (PKC) in skeletal muscle;
| this in turn triggers a cascade of kinase activities that compromises
| insulin signaling by phosphorylating a key serine group (S307 in rats,
S312
| in humans) in IRS-1, rendering this crucial intermediate a less suitable
| substrate for the activated insulin receptor [6-10].
|
|
| Med Hypotheses. 2006;66(3):527-34. Epub 2005 Nov 23.
| Induction of heat shock proteins may combat insulin resistance.
|
| The molecular mechanism responsible for obesity-associated insulin
| resistance has been partially clarified: increased fatty acid levels in
| muscle fibers promote diacylglycerol synthesis, which activates certain
| isoforms of protein kinase C (PKC). This in turn triggers a kinase
cascade
| which activates both IkappaB kinase-beta (IKK-beta) and c-Jun N-terminal
| kinase (JNK), each of which can phosphorylate a key serine residue in
IRS-1,
| rendering it a poor substrate for the activated insulin receptor. Heat
shock
| proteins Hsp27 and Hsp72 have the potential to prevent the activation of
| IKK-beta and JNK, respectively; this suggests that induction of heat
shock
| proteins may blunt the adverse impact of fat overexposure on insulin
| function. Indeed, bimoclomol--a heat shock protein co-inducer being
| developed for treatment of diabetic neuropathy--and lipoic
acid--suspected
| to be a heat shock protein inducer--have each demonstrated favorable
effects
| on the insulin sensitivity of obese rodents, and parenteral lipoic acid
is
| reported to improve the insulin sensitivity of type 2 diabetics.
Moreover,
| there is reason to believe that heat shock protein induction may have a
| favorable impact on the microvascular complications of diabetes, and on
the
| increased risk for macrovascular disease associated with diabetes and
| insulin resistance syndrome. Heat shock protein induction may also have
| potential for preventing or treating neurodegenerative disorders,
| controlling inflammation, and possibly even slowing the aging process.
The
| possible complementarity of bimoclomol and lipoic acid for heat shock
| protein induction should be assessed, and further efforts to identify
| well-tolerated agents active in this regard are warranted.
|
| PMID: 16309849
|
| hth
| Gys
|
|


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