SIRT1, a protein that slows down the aging of mice and other animals, may protect against the harmful effects of a high-fat diet, including the development of diabetes, according to a study by scientists at the Massachusetts Institute of Technology (MIT).
The long-life-promoting properties of the SIRT1 protein were discovered in the 90s by MIT biology professor Leonard Guarente during research on yeast. Since then, he has been analyzing its role in various tissues. Thanks to this, he determined, among others, that this protein protects against neurodegenerative changes accompanying Alzheimer’s, Parkinson’s and Huntington’s diseases. In recent work, Guarente has focused on the impact of SIRT1 on the development of obesity-related diseases.
When the gene encoding SIRT1 was turned off in the adipocytes of mice and fed with high-fat food, metabolic disorders and diabetes began to develop much earlier than in the control group of rodents that received the same food. This means that SIRT1 acts as a protection in adipocytes (cells that synthesize and store simple fats).
SIRT1 belongs to the so-called deacetylases, i.e. proteins that remove acetyl groups and modify the activity of genes. In mice that were not deprived of the SIRT1 protein, a high-fat diet activated most of the same genes as in mice without SIRT1 receiving normal food.
In normal high-fat-fed mice, the SIRT1 protein is broken down by an enzyme called caspase-1, which is involved in inflammation. We already know that a high-fat diet can promote inflammation, but it’s not entirely clear how. Our research shows that the consequence of triggering an inflammatory response is the breakdown of the SIRT1 protein in fat cells, says Guarente.
Scientists speculate that drugs that activate SIRT1 could help protect patients at risk from obesity-related diseases (PAP).
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