Obesity is a slow suicide
How Obesity Kills the HeartKirill Stasevich, Compulenta
In heart failure, which occurs due to obesity, special regulatory molecules of small nucleolar RNAs are "guilty", which, with an increase in the concentration of fatty acids in the cell, trigger the procedure of cellular suicide.
When we eat more than we should, special adipocyte cells come to the rescue. They "catch" excess fat traveling through the bloodstream, storing it in themselves; these cells mainly make up adipose tissue. But adipocytes cannot always cope with the amount of calories that our diet is sometimes so rich in, and in this case other cells will connect to adipocytes, also starting to store excess fats.
The problem is that other cells are not very adapted to perform such a function, and the excess of lipids entering them disrupts the work of genes, intracellular metabolism and triggers the procedure of cellular suicide. And mass cell death, in turn, can lead to kidney or heart failure.
Researchers from Washington University in St. Louis (USA) have discovered a gene that triggers cell death when it "overeats". It is called rpL13a, but in this case we are not talking about the protein that this gene encodes. In the rpL13a sequence, there are sections of DNA that are copied into molecules of so-called small nucleolar RNAs. These RNAs do not serve for the synthesis of polypeptides, but are regulatory molecules that perform chemical modifications of RNAs of other classes (such as ribosomal or transport RNAs), thereby affecting their functioning.
As researchers write in the journal Cell Metabolism (Michel et al., Small Nuclear RNAs U32a, U33, and U35a Are Critical Mediators of Metabolic Stress), excess fatty acids in the cell increased the activity of the rpL13a gene: more protein encoded by rpL13a and more nucleolar RNAs were formed in the cell. But at the same time, it was the nucleolar RNAs that triggered the cell suicide procedure: if the rpL13a gene was turned off in the cells, suicide was postponed, but if three types of RNAs encoded by the rpL13a site were injected into such cells, the function of programmed death was restored. If the activity of small nucleolar RNAs was blocked in the cells, they became resistant to a variety of stresses, and not only to an increased content of fatty acids. The fluorescent label attached to these RNAs made it possible to detect their transition into the cellular cytoplasm, that is, the functions of small nucleolar RNAs are not at all limited to that zone of the nucleus, which is commonly called the nucleolus and in which the synthesis of ribosomal RNA particles takes place.
When a large amount of fatty acids enters the cell, small nucleolar RNAs (red)
they leave the nuclei (green) and go to the cytoplasm, where they start the cell suicide procedure
(photo of the authors of the work)
The cell death program is activated when a cell receives significant genetic damage and begins to pose a threat to its neighbors. But it also happens that the same program starts working unnecessarily, reacting to some extraneous signal. In this case, such a signal turns out to be an excess of fatty acids arriving "at the wrong address".
The discovery of a new class of molecules that trigger unpleasant side effects from overeating and overweight will allow the creation of drugs that protect tissues and organs from unnecessary damage that they can inflict on themselves. Although, of course, no matter how significant the successes of scientific and technological progress may be, they do not at all cancel the need to be more moderate in food.
Prepared based on the materials of Washington University in St. Louis: Surprising culprits behind cell death from fat and sugar overload.
Portal "Eternal youth" http://vechnayamolodost.ru07.07.2011