Study Shows Connection Between Longevity Boosting Protein and Diabetes

 Longevity Boosting Protein and Diabetes

A new study led by a research team from the Massachusetts Institute of Technology (MIT) reveals that a protein that is responsible for slowing down the aging process in laboratory mice might also have an effect against diabetes.

More than 10 years ago, biology professor Leonard Guarente, from MIT, discovered the anti-aging properties of the SIRT1 (Silent Information Regulator) gene, which is found in sirtuin proteins. In his most recent study, published in the journal Cell Metabolism, on the 8th of August, he examined what happens if the gene is missing from the adipose cells (the cells which make up the body fat).

For these results, the team used laboratory mice, which were kept on high-fat meals. The mice which were lacking the SIRT1 protein were found to develop several metabolic disorders, including diabetes, whilst the mice who weren’t lacking the protein developed these disorders later in time.

“We see them as being poised for metabolic dysfunction. You’ve removed one of the safeguards against metabolic decline, so if you now give them the trigger of a high-fat diet, they’re much more sensitive than the normal mouse”, said professor Guarente.

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 The results of the study suggest that medication what enhances the activity of the SIRT1 protein could be used to treat metabolic diseases linked to obesity. Professor Guerente is the one who discovered the effects of both SIRT1 and other sirtuin proteins. The role of the sirtuin proteins is to keep the cells alive through the coordination of regulatory proteins, hormonal networks and the coordination of other genes.

Professor Guarente and his research team deleted the gene from the brain and the liver in order to better study its effects. Previous studies have shown that SIRT1 protects against the neurodegeneration that comes along with diseases such as Alzheimer’s, Parkinson’s or Huntington’s. The team of researchers has shown that the protective abilities of the SIRT1 protein are obtained through the process of deacetylation.

The team found that a high percentage of the hundreds of genes that were studied in the mice lacking the SIRT1 protein (which were on a normal diet) were also found in the normal mice that received a high-fat diet. Professor Guarente says that the results of his study suggest that the onset of metabolic disorders is composed of two steps, the first step being the inactivation of the SIRT1 protein.

A closer look into the process revealed that the SIRT1 protein is proteolitically cleaved by the caspase-1 enzyme. This enzyme is also related to inflammation, whether it’s induced by high-fat diets or not. However, the process through which high-fat diets induce inflammation is still unknown.

“What our study says is that once you induce the inflammatory response, the consequence in the fat cells is that SIRT1 will be cleaved”, said professor Guarente.