Obesity caused mitochondria to break down into pieces

Overweight remains one of the main health problems, so scientists are actively studying the mechanisms of its development. This time they paid attention to mitochondria - organelles called "power plants" of the cell - and found out that in mice on a fat diet they are destroyed into fragments. This involves a protein called RalA, which, by acting on it, can alter fat metabolism and prevent excess weight gain.

Obesity and overweight is one of the most common health problems that has become a real scourge in many developed countries. For example, in the United States, 35 percent of men are overweight and 40 percent are obese.

Excess weight has a detrimental effect on many organs and is associated with a host of diseases, including heart disease, hypertension, diabetes, chronic inflammation and the so-called metabolic syndrome. Accordingly, the molecular mechanisms by which excess adipose tissue spoils health are also diverse.

The authors of a new paper for the journal Nature Metabolism focused on the changes that occur against the background of obesity in mitochondria. These "energy stations" of the cell provide oxidation of organic compounds and the production of energy stored in the form of ATP molecules. Organelles, in particular, are responsible for the rapid "burning" of fats, which avoids the growth of their reserves in the body.

However, in obesity, which disrupts many body functions, mitochondria also begin to "break down". To study this process, scientists put male laboratory mice on a fat-rich diet. It turned out that the abuse of fat leads to the breakdown of mitochondria of white adipose tissue cells into parts - that is, fragmentation. Because of this, the organelles began to work worse and could not properly oxidize the products of metabolism, which is fraught with an increase in the problem of overweight.

Then the scientists found out that the fault of the destruction of mitochondria was the activation of the enzyme RalA, which belongs to the group of GTPases. In particular, the protein is able to "turn on" another enzyme (Drp1) that stimulates the breakdown of mitochondria. Biologists therefore hypothesized that "turning off" RalA by gene knockout would help keep mitochondria functioning normally. They obtained mice with a deletion of this gene - removing part of the rodents' DNA sequence.

The mice with the altered genome acquired a kind of immunity to obesity and its consequences. On the background of excessive fatty foods, they gained weight much less (compared to the control group). Moreover, these animals did not have such signs of diabetes as increased insulin levels and violations of the concentration of glucose and triglycerides in the blood.

The authors of the study emphasized that a similar RalA enzyme exists in humans. It may well become a new target for the therapy of obesity and overweight, preventing many cases of disease and death in the future.