Protein sirtuin protects against the destructive effect of high-fat diet and obesity
Last reviewed: 23.04.2024
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A new study by the Massachusetts Institute of Technology (MIT) suggests that the sirtuin protein, which slows down the aging process of many animal species, protects against the destructive effect of high-fat diets and diseases associated with obesity, including diabetes .
Professor of biology MIT Leonard Guarente (Leonard Guarente) discovered the ability of the protein SIRT1 to increase the life expectancy of some species of animals more than ten years ago and has since studied its role in many different tissues. In a recent study published in the print edition of Cell Metabolism, he showed what happens when there is no SIRT1 protein in adipocytes-cells that make up adipose tissue.
In the absence of this protein in mice that are on a diet high in fat, metabolic disorders begin to develop much earlier than in normal animals that receive the same food.
This discovery suggests that drugs that increase the activity of SIRT1, can protect against diseases associated with obesity.
Professor Garente discovered the effects of SIRT1 and other sirtuins in the study of yeast in the 90s of the last century. Since then, scientists have proven the vital role of these proteins in the coordination of various hormonal networks, regulatory proteins and other genes that help maintain the healthy state of the cell.
In recent years, Garente and his colleagues have focused on the effects of removing this gene from brain cells and the liver. Their previous work showed that SIRT1 protects the brain from degeneration, characteristic of Alzheimer's, Parkinson's and Huntington's diseases.
Protein SIRT1 removes acetyl groups from other proteins, changing their activity. There are many targets of this deacetylation, which probably explains the wide range of protective effects of SIRT1.
Professor of biology MIT Leonard Guarente (Leonard Guarente) discovered the effects of SIRT1 and other sirtuins in the study of yeast in the 90s of last century. His latest discovery suggests that drugs that increase the activity of SIRT1, can protect against diseases associated with obesity.
In the latest study, the researchers analyzed hundreds of genes included in mice that were deprived of SIRT1 but were on a normal diet, and found that they were almost identical to those included in normal mice on a diet high in fat.
This means that in normal mice the development of metabolic disorders is a two-stage process. "The first stage is the inactivation of SIRT1 high in fat, and the second stage is all the bad things that follow the first," Garente comments on the results of his work.
Scientists have studied how this happens, and found that in normal mice fed high-fat foods, the SIRT1 protein is cleaved by the caspase-1 enzyme, induced by inflammation. It is known that diets with a high fat content can provoke the development of inflammation, although it is not yet clear how.
"Our study shows that in fat cells an unavoidable consequence of the induced inflammatory reaction is the cleavage of SIRT1," the scientist continues.
According to Anthony Suave, an associate professor of pharmacology at Weill Cornell Medical College who did not participate in this study, this discovery "offers a good molecular mechanism that explains how inflammatory signals in adipose tissue can quickly lead to dysfunction of metabolic tissue. "
The drugs, whose target is the inflammatory process, as well as increasing the activity of sirtuins, may have some positive therapeutic effect on obesity-related diseases, says Dr. Svejv.
In addition, the researchers found that with aging in normal mice, the sensitivity to the effects of a diet high in fat increases, which means that in the aging process the protective effect of sirtuins is lost. It is known that aging strengthens inflammation, and Professor Garente is now studying whether SIRT1 is provoked by this inflammation associated with aging.
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