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Longevity Briefs: A Single Bout Of Exercise Can Improve Blood Sugar

Posted on 12 May 2021

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Longevity briefs provides a short summary of novel research in biology, medicine, or biotechnology that caught the attention of our researchers in Oxford, due to its potential to improve our health, wellbeing, and longevity.

Why is this research important: Insulin resistance is a common metabolic disorder in which cells don’t respond as well to the blood sugar lowering hormone insulin. Insulin gets released from the pancreas in response to a rise in blood glucose (sugar). In response, cells insert special transport proteins into their membranes, allowing glucose to move from the blood into cells where it is used or stored.

In insulin resistance, fewer of these transport proteins are inserted in response to a given amount of insulin. This means that more insulin is required to achieve a given reduction in blood sugar. In humans, muscle is thought to be the first tissue to become insulin resistant, meaning that the liver must compensate by taking up the excess glucose and converting it into fat. However, the liver eventually becomes insulin resistant as well, and the pancreas no longer produces enough insulin to keep blood sugar in check.

What did the researchers do: In this study, researchers investigated insulin resistance in the muscle, and fat metabolism in the liver, in response to exercise. 12 insulin resistant, but otherwise young and healthy volunteers were given a carbohydrate meal. Researchers then used nuclear magnetic resonance techniques to measure glycogen (a form of stored glucose) and fat content in the liver and muscle when the subjects either rested or exercised for 45 minutes prior to their meal.

Key takeaway(s) from this research: The subjects who exercised produced over three times as much muscle glycogen following their meal compared those who did not exercise, and had a roughly 40% reduction in fatty acid production in their livers. These differences were independent of any changes in insulin concentrations, suggesting that those who exercised either experienced increased sensitivity to insulin, or that transport of glucose into their muscle cells increased independently of insuliln.

One plausible explanation is that exercise activates a molecule called AMPK, which has been shown to promote the insertion of glucose transporters into the cell membrane without the need for insulin. Exercise, even in a single bout, may therefore ‘bypass’ insulin resistance.

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      Reversal of muscle insulin resistance with exercise reduces postprandial hepatic de novo lipogenesis in insulin resistant individuals:

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