This article was published in Scientific American’s former blog network and reflects the views of the author, not necessarily those of Scientific American
In addition to helping us get fit, exercise seems to play a disproportionate role in fending off chronic diseases, such as diabetes. A new study suggests how activity on the cellular level might be keeping us healthy when we get activity on the macro level.
The process in question is autophagy, a series of actions in which cells recycle internal bits and that, in turn, helps to keep cells agile and able to adjust to changes in energy requirements and nutritional conditions. Exercise kicks autophagy—in heart and skeletal muscles—into high gear in mice. And the new report, published online Wednesday in Nature, describes how this extra autophagy seems to help keep insulin resistance (a precursor to diabetes) at bay in the lab rodents (Scientific American is part of Nature Publishing Group).
The research team, led by Congcong He, of the University of Texas Southwestern Medical Center, compared mice that had been genetically engineered so that they did not get the autophagy boost to regular mice to see how each fared after exercise and a high-fat, diabetes-promoting diet. Mice without the natural levels of exercise-induced autophagy gained a little more weight on the high-fat diet and were slightly less active than their natural-bread counterparts. And perhaps more important, while the regular mice saw an improvement in their diet-related insulin resistance when they were exercised—making them less likely to get diabetes—the mutant mice who did not undergo the extra autophagy did not seem to get these exercise benefits.
On supporting science journalism
If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.
"Our findings demonstrate that exercise is a potent inducer of autophagy," the researchers wrote. "Autophagy induction may contribute to the beneficial metabolic effects of exercise," they concluded.
The team also found that this cellular autophagy is controlled in part by a particular protein, BCL2, which other researchers have found plays a key role in cell death. Manipulating this protein "may be a logical strategy to mimic the health effects of exercise and to prevent or treat impaired glucose metabolism," the researchers suggested.
Of course it would be a long way from these running lab mice to finding a related treatment for human diabetes, but the new find is just one of many recent clues scientists have gathered in an effort to better understand exercise and how its biochemical effects might help prevent metabolic diseases. Just last week, another team of researchers announced the discovery of irisin, a new exercise-induced hormone in humans and mice that seems to help burn extra calories and also improve insulin sensitivity.