Anti-aging Protein May Hold Off Diabetes

After a research team at MIT put mice on a high fat diet, they observed something interesting. Those mice that were missing a certain anti-aging protein quickly developed metabolic disorders, including diabetes, while mice that had the protein did not.

More than 10 years ago MIT researcher Leonard Guarente identified the SIRT1 protein and since then has continued to study its effects on human and animal biology. His research on sirtuin proteins, like SIRT1, started in the 1990s and since then they have been shown to, “help keep cells alive and healthy by coordinating a variety of hormonal networks, regulatory proteins, and other genes.”(Medical News Today) His most recent findings appear in this week’s issue of the medical journal called Cell Metabolism.

Unraveling Past Research

Previous research from the Washington University School of Medicine, Department of Developmental Biology discusses the role that SIRT1 and another compound called nicotinamide phosphoribosyltransferase, or NAMPT, have in treatment of type 2 diabetes. Researchers are just beginning to understand how this anti-aging protein works to balance glucose levels. In 2009, the National Institutes of Health published findings that said:

In pancreatic beta cells, SIRT1 promotes glucose-stimulated insulin secretion and might contribute to beta cell adaptation in response to insulin resistance. In the liver, SIRT1 regulates glucose production … and appears to regulate insulin sensitivity negatively. In skeletal muscle, SIRT1 might play an important role in improving insulin sensitivity by increasing fatty acid oxidation … SIRT1 promotes fatty acid mobilization… The total effect of SIRT1 in white adipose tissue on insulin sensitivity is still unclear.

This new research just starts to unravel the mystery of the SIRT1 protein’s role in glucose management and insulin resistance. It is known that inflammation increases with age. Guarente is now studying to see if there is an inverse relationship between inflammation and loss of the SIRT1 protein.

Sources:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2734392/?tool=pubmed
http://www.medicalnewstoday.com/articles/248742.php