Researchers at the Max Planck Society have determined that the protein FKBP51 may act as a molecular link between the stress response system and metabolic processes within the body. They also described autophagy as the central mechanism involved.
The study appeared in the journal Science Advances.
“Autophagy is the cell’s recycling program, which gets rid of old or damaged proteins. As such, it can counteract aging processes and—as we have now been able to show—reduce obesity,” according to one expert who heads the Neurohomeostasis Research Group.
Another expert mentions in the same news release: “The fact that the stress factor FKBP51 in the brain is a master regulator of autophagy and thus obesity reveals a number of new intervention possibilities, from pharmacological manipulation of FKBP51 to autophagy-inducing fasting diets or sports programs.”
The findings indicate how mediobasal hypothalamus FKBP51 deletion can dramatically induce obesity. Its overexpression, on the contrary, can protect against high-fat diet-induced obesity.
“Our study provides an important novel regulatory function of MBH FKBP51 within the stress-adapted autophagy response to metabolic challenges,” said the researchers in their journal release.