How does exercise accelerate glucose uptake in diabetes?

[sodium.dioxid]

We're usually just told that exercise is a great way to stimulate the movement of glucose into cells. But how does it do that? I would think that insulin resistance is insulin resistance, exercise or no exercise.

 

[Yanick]

It's fairly complicated but the take-away is that there are multiple mechanisms for improving blood sugar control, insulin sensitivity being a piece of the puzzle.

http://stke.sciencemag.org/cgi/content/abstract/vj_pnas;97/1/38

 

[SW VandeCarr]

It's fairly complicated but the take-away is that there are multiple mechanisms for improving blood sugar control, insulin sensitivity being a piece of the puzzle.

http://stke.sciencemag.org/cgi/content/abstract/vj_pnas;97/1/38

This study (above), while interesting and informative, does not specifically address the issue of insulin resistance in humans. It's long been held that diet and exercise with weight loss can at least partially reverse insulin resistance. The linked study below does demonstrate that a single bout of exercise can decrease de novo hepatic production of lipids and triglycerides after a high carbohydrate meal as it reverse skeletal muscle insulin resistance in human volunteers. Insulin resistance is present before the appearance of overt type 2 diabetes and its early reversal with diet and exercise may prevent its development.

http://www.pnas.org/content/108/33/13705.full

"In this regard, insulin resistance, localized to skeletal muscle, has been hypothesized to cause atherogenic dyslipidemia and NAFLD by changing the pattern of storage of ingested carbohydrate away from skeletal muscle glycogen synthesis into hepatic de novo lipogenesis, resulting in an increase in plasma triglyceride concentrations, reduction in plasma high-density lipoprotein concentrations and increased liver triglyceride synthesis in healthy, young, lean insulin resistant individuals (3). This hypothesis has important implications for the treatment of hyperlipidemia and NAFLD associated with the metabolic syndrome in that it implicates skeletal muscle insulin resistance as a primary therapeutic target."

NAFLD: Non alcoholic fatty liver disease.

 

[Yanick]

This study (above), while interesting and informative, does not specifically address the issue of insulin resistance in humans. It's long been held that diet and exercise with weight loss can at least partially reverse insulin resistance. The linked study below does demonstrate that a single bout of exercise can decrease de novo hepatic production of lipids and triglycerides after a high carbohydrate meal as it reverse skeletal muscle insulin resistance in human volunteers. Insulin resistance is present before the appearance of overt type 2 diabetes and its early reversal with diet and exercise may prevent its development.

http://www.pnas.org/content/108/33/13705.full
NAFLD: Non alcoholic fatty liver disease.

I agree, though I haven't read the paper(s) very carefully. Very busy lately. My point was simply to show how complicated glucose homeostasis can be especially in the context of exercising. My introduction into science came through fitness/bodybuilding/powerlifting/Olympic lifting, so I am aware, if not fully up to date, on the complexities of topics such as the one here.

 

[SW VandeCarr]

I agree, though I haven't read the paper(s) very carefully. Very busy lately. My point was simply to show how complicated glucose homeostasis can be especially in the context of exercising.

It's a good paper. The fundamental problem seems to be a relative deficiency of skeletal muscle glycogen with insulin resistance. Research seems to have focused on three likely targets for possible therapeutic intervention regarding intracellular mechanisms for insulin resistance: glycogen synthase, hexokinase II (involved in producing glucose-6 phosphate) and glucose transport. The weight of the evidence according to this article (below) favors the last as the rate limiting step in glycogen synthesis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC314317/

Your article focused on glucose transporters, particularly GLUT4 and also insulin receptor substrates (IRS1 and IRS2). I also found an article in the Wikipedia regarding GLUT4 which states that GLUT4 tends to move to the cell surface from the interior with muscle contraction. This would establish a direct link between exercise and intracellular glucose transport. I don't usually link to the Wiki, but this short article is easy to read, is well referenced and carries no warnings from Wiki editors.

http://en.wikipedia.org/wiki/GLUT4