Researchers at the Dana-Farber Cancer Institute and Harvard Medical School have discovered a new hormone produced in response to exercise that may be turning people’s white fat brown, and in the process decreasing the likelihood that they will develop diabetes, obesity, heart disease, and other health problems. The study, published 1/11/12 in the journal Nature, provides new insights on how the body responds to exercise at the cellular level. Scientists have believed for years that muscle cells communicate with other cells during and after exercise; in particular, fat cells. But the how and what they say have been mysteries, until, in the new study, they looked at a particular substance, PGC1-alpha, which is produced in large quantities during and after exercise. Bruce Spiegelman, professor of cell biology and medicine and the Dana-Farber Cancer Institute and Harvard Medical School, led the study. He says that “It seems clear that PGC1-a stimulates many of the recognized health benefits of exercise.” Mice that are bred to produce large amounts of PGC1-a in their muscles are more resistant to age-related obesity and diabetes, much like humans who exercise. One thing that PGC1-a does is pump up the expression of a protein, Fndc5, which breaks apart into different pieces, one of which is a hormone called irisin, which enters the bloodstream and surfs to fat cells. There, it begins turning regular fat, especially the deep, visceral fat around organs-into brown fat. Brown fat is the “good” fat-it is metabolically active, using oxygen and energy. End result, they burn calories. White fat, or “bad’ fat, just sits there, causing metabolic problems. In essence, irisin appears to be one of the more important missing links in our understanding of how exercise conveys health benefits. What is not known at this point is how much or what types of exercise produce the greatest natural irisin increases in healthy people. Until then, some exercise is better than none. A follow-up on yesterday’s blog on the brain: A new study from The Archives of Neurology suggests that for some people, a daily walk or jog could reduce the risk of developing Alzheimer’s or change the course of the disease if it begins. In this study, researchers at Washington University in St. Louis recruited 201 adults, ages 45-88, who were part of continuing study at the university’s Knight Alzheimer’s Disease Research Center. Some had a family history of Alzheimer’s, but none, as the study began, had the disease. All performed well on tests of memory and thinking. At the beginning of the experiment, all volunteers had their brains scanned using positron emission tomography (PET scan), to look for signs of amyloid plaques in the brain, a hallmark of Alzheimer’s. People with a lot of plaque have more memory loss. Next they tested them for APOE, a gene involved in cholesterol metabolism. Everyone carries the APOE gene, but those who have a particular version of the gene known as e4 are at 15 times the risk of developing Alzheimer’s as those who don’t. In this study, 56 of the volunteer’s turned out to be positive for APOE-e4. All participants were asked to fill out detailed questionnaires about their exercise habits during the past 10 years. For the group as a whole, exercise provided marginal benefits-the ones who reported walking or jogging often, had fewer amyloid plaques than those who almost never did, but the difference was insignificant. However, when the scientists examined the results for the people with the e4 gene variant, the situation changed. Those that exercised had plaque accumulation similar to those who were e4 negative. Bottom line; activity levels enable those with the genetic predisposition to get Alzheimer’s to ‘turn off’ that gene, and stand a greater chance of aging normally. For a more complete account of these two studies, read Gretchen Reynolds, The New York Times-Phys ED column.
Stay well, John R Blilie, M.S.