The protein released by fat after exercise improves glucose

It is well known that exercise improves health, but researchers at the Joslin Diabetes Center answer the question of how they improve their health at the molecular level.

After conducting experiments on humans and mice, the researchers found that physical training resulted in dramatic changes in fat. In addition, they have discovered that this "entrained" fat releases into the blood factors that can have positive health effects. The study was published online on February 11, 2019 in Metabolism of nature.

It is known that fat cells secrete proteins called adipokines and that many adipokines increase with obesity, which has harmful effects on metabolism and health.

"In contrast to the negative effects of many adipokines, our study identified transforming growth factor beta 2 (TGF-beta 2) in the form of an adipokine released by adipose tissue (fat) in response to exercise that improves actually glucose tolerance, "says Laurie J. Goodyear, Ph.D., head of the Josi section on Integrative Physiology and Metabolism and co-author of the study.

Exercise-stimulated TGF-beta 2 has not only improved glucose tolerance, but treatment of obese mice with TGF beta 2 has lowered blood lipid levels and improved many other aspects of metabolism.

"The fact that a single protein has such dramatic and dramatic effects was pretty impressive," says Goodyear, a professor of medicine at Harvard Medical School.

Two years ago, the international research team demonstrated for the first time that adipose tissue offers beneficial metabolic effects in response to exercise.

"Our hypothesis was that exercise alters adipose tissue and that as a result of this change, lipid releases these beneficial proteins into the bloodstream," Goodyear said. "Before this discovery, we have always focused on the positive effects of muscle."

Ssuking this information, Joslin researchers sought to identify adipokines released by fat during exercise. To do this, they conducted a series of molecular experiments in humans and mice. They identified levels of adipokines in men before and after an exercise cycle. They also studied exercise mice.

Their badysis identified TGF beta 2 as one of the positively regulated proteins in exercise in humans and mice. Further investigations confirmed that levels of this adipokine actually increased in adipose tissue as well as in blood during exercise, in both cases.

To find out if the protein resulted in beneficial metabolic beneficial effects, they treated mice at TGF beta 2. The experiment showed a number of positive metabolic effects in mice, including improved tolerance to glucose and increased absorption of fatty acids.

Then, they fed the mice with a high-fat diet, which caused the development of diabetes in animals. To find out if TGF beta 2 was actually responsible for the metabolic effects, they treated diabetic mice with TGF beta 2. This reversed the negative metabolic effects of the high-fat diet, as was the case with exercise .

"Our results are important because it is actually the first demonstration of an adipokine released to stress that may have beneficial metabolic effects on the body," says Goodyear.

Another important discovery is that lactic acid, released during exercise, is an integral part of the process. Lactate is released by the muscles during exercise and then moves to the fat where it triggers the release of TGF beta 2.

"This research is truly revolutionizing the way we think about exercise and the many metabolic effects of exercise, and most importantly, this fat actually plays an important role in the functioning of exercise," he says. Goodyear.

These results suggest that TGF beta 2 might be a potential therapy for the treatment of hyperglycemia, and possibly a treatment for type 2 diabetes. Long-term studies will be needed to determine the safety of treatment by TGF beta 2.

Provided by
Joslin Diabetes Center