The proteins released by fat after exercise can improve glucose

As we all know, exercise make us stronger and healthier. But do you learn how exercise helps us healthy on a molecular level? 

Researchers at Joslin Diabetes Center answered the question in a study that published online February 11, 2019, in Nature Metabolism. The study showed that fats in the body after exercise release a protein into the bloodstream, which has a positive impact on health. 

Fat cells secrete dozens of cytokines, such as leptin, adiponectin, acylation stimulating protein, omentin, and cytokines, collectively known as adipokines. As people become fatter, many adipokines in their bodies are harmful effects on metabolism and health. 

Under physiological conditions, adipokines act mainly on adipose tissue (paracrine or autocrine) or through blood circulation to distant target organs, regulating their growth and development, metabolism and tissue remodeling. 

However, under pathological conditions, such as obesity and metabolic syndrome, the synthesis and secretion of adipokines are disordered. The endocrine function of obese adipose tissue is focused on the negative metabolic effects caused by excess adipose tissue. The main consequence is the promotion of diabetes and the occurrence of obesity-related diseases such as atherosclerosis. Obesity is closely related to insulin resistance, hyperglycemia, low inflammation, dyslipidemia, and metabolic syndrome (MS).

Contrary to the negative effects of many adipokines, this study identified TGFB2 (transforming growth factor beta 2) as adipokines released by adipose tissue (fat) in response to exercise that actually improves glucose tolerance.  

Two years ago, the international research team first demonstrated that adipose tissue provides beneficial metabolism during exercise. But at that time, experts were focused on the positive effects of muscles.

The researchers assumed that exercise is altering fat, based on the change, the fat release beneficial proteins into the bloodstream. 

In order to find out the adipokines released by fats during exercise, the researchers performed a series of molecular experiments on humans and mice. They determined the level of adipokines in men and mice before and after the exercise cycle, finding that TGFB2 is one of the up-regulated proteins in humans and mouse movement. In addition, other studies have confirmed that in both cases, levels of this adipokines actually increase in adipose tissue and in blood flow during exercise.

Next, they dealt with mice with TGFB2 to test whether the proteins promote beneficial metabolism. These treated mice showed many positive metabolisms, including improved glucose tolerance and increased intake of fatty acids.

Flowing, they fed the mice with high-fat food, which finally caused the mice to develop diabetes. And then, they treated diabetic mice with TGFB2 to see if it is really responsible for metabolism. This reversed the negative metabolic effects of a high-fat diet, just like exercise. 

Surprisingly, they also found that lactic acid released during exercise is an integral part of this process. Lactic acid is released by muscles during exercise and then enters into fat, where it triggers the release of TGFB2.

These finding indicated that TGFB2 may be a potential therapy for hyperglycemia and finally for type II diabetes. And long-term studies are needed to determine the safety of TGFB2 therapy.