There’s a way to slow down metabolic aging

Brown adipose tissue is a unique type of fat that is able to produce heat by burning excess energy. It protects the body from obesity, type 2 diabetes, and heart disease. Unlike white fat, which stores energy, brown fat consumes it by converting calories into heat.

However, with age, its activity decreases noticeably. Until now, the reasons for this have been unclear. A new animal experiment has shown that a key role is played by a process called chaperone-mediated autophagy (CMA), the mechanism by which cells dispose of unnecessary proteins.

It was found that in a young body, CMA actively works by purifying the cells of brown adipose tissue from proteins that inhibit its thermogenic activity. With age, this mechanism weakens, and excess proteins begin to accumulate, preventing fat from performing its functions.

“We found that a decrease in CMA is directly related to a decrease in the activity of brown adipose tissue. So, if you influence this process, you can restore its work,” explains Professor Villarroya.

As part of the experiment, elderly mice were injected with drugs that stimulate CMA, the same drugs that are being developed to treat neurodegenerative diseases associated with the accumulation of pathological proteins. The results turned out to be interesting: brown fat in aging animals retained its activity, and metabolism improved.

So far, we are talking about preclinical trials, but the researchers are confident that this approach can become the basis for the development of drugs that prevent age—related decline in brown fat and related problems such as obesity, diabetes and cardiovascular disorders. If the results are confirmed in humans, medicine will receive a new tool for preventing diseases of aging and combating the epidemic of obesity.

“We are already exploring how activating CMA can help increase energy expenditure and prevent metabolic disruptions in humans,” adds Villarroya.