microRNAs and obesity

Key Molecular "fat storage" Found

Ksenia Vasilyeva, Vesti

Obesity is not just an aesthetic flaw and the inability to "fit" into the clothes you like or the standard sizes of airplane seats, trains and cinemas. Unfortunately, this is a serious disease that has long been a global health problem. And it is not surprising, because excess fat is a serious risk of developing type 2 diabetes, cardiovascular diseases, stroke and even cancer.

The genetic and molecular mechanisms responsible for the amount and places of fat deposition in the body are the alpha and omega of understanding the processes of obesity. However, so far these hidden processes remain not fully understood.

Recently, experts from the Southwest Texas University Medical Center found that a key role in the development of obesity is played by one of the families of microRNAs, namely miR-26.

Let's explain that microRNAs are small non–coding RNA molecules. They are able to influence the activity of genes, suppressing their work.

In animal experiments, scientists have found that the miR-26 family controls the level of one of the proteins necessary for the production of new fat cells.

"Previously, this protein was not associated with the formation of fat or obesity, so the result we obtained was very unexpected," Professor Joshua Mendell, one of the lead authors of the new study, notes in a press release.

Let us explain that the varieties of microRNAs have long been of interest to geneticists. Previous studies have already demonstrated the important role of the miR-26 family in suppressing malignant tumors and regulating insulin sensitivity.

However, the broader functions of these microRNAs remained unknown. The fact is that for a detailed study of these molecules in mammals, it is necessary to isolate three genes encoding the entire miR-26 family, and this is not easy to do.

To overcome such a technical obstacle, the researchers used the CRISPR/Cas9 gene editing technique. With its help, scientists removed all the genes encoding miR-26 from the mouse genome. The "operation" helped the experts to discover a curious phenomenon.

Mice with missing miR-26 microRNAs developed quite normally in childhood. However, as they grew older, they began to overtake their usual peers two or three times in terms of the amount of white fat in the body (the same that forms annoying volumes on the abdomen, thighs and buttocks). And this is despite a normal balanced diet.

To study the role of miR-26 in fat formation, scientists used another genetically engineered line of mice. This time, the body of the experimental subjects produced an excess of the microRNA of interest to scientists.

Next, the researchers fed the modified and control group of ordinary rodents with fatty foods. As expected, normal animals experienced a sharp increase in weight and an increase in fat content up to 40 percent of the total body weight. But their genetically transformed "colleagues" had a completely different situation.

Mice with elevated levels of miR-26 were very resistant to weight gain and, despite an identical diet, practically did not get fat. Scientists also note that these subjects had lower levels of sugar and lipids in the blood compared to the control group.

"Our study reveals a new mechanism for controlling the production of fat in the body. A deeper understanding of this process will lead to the emergence of new methods of treating obesity, for example, by increasing the activity of miR-26 or suppressing the targets of this microRNA," says Professor Mendell.

Detailed results of the study were published in the publication Genes & Development (Acharya et al., miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19).

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