Stress-Induced Gene Revealed as Key Player in Diabetes Development

Researchers from Osaka Metropolitan University have uncovered a critical genetic mechanism linked to the development of type 2 diabetes. The study focuses on a gene called REDD2, which is activated under metabolic stress conditions—such as high glucose levels, elevated fatty acids, and exposure to diabetogenic chemicals. When this gene is overexpressed, it causes damage to pancreatic β-cells, the cells responsible for insulin production and blood sugar regulation. This damage impairs insulin secretion, leading to elevated blood glucose levels and the progression toward diabetes.

The research found that under stress, REDD2 activity increases, resulting in the suppression of the mTORC1 pathway, a vital cellular growth and survival pathway. Suppressing REDD2 in both cell cultures and animal models improved β-cell survival and function, even in conditions mimicking high-fat diets and chemical-induced diabetes. Mice deficient in REDD2 showed better blood sugar control, greater numbers of healthy β-cells, and increased insulin production. Human islet studies supported these findings, highlighting REDD2's negative influence on β-cell mass and insulin secretion.

This discovery opens new therapeutic avenues for early detection and treatment of type 2 diabetes. Targeting REDD2 could not only prevent β-cell damage but also serve as a diagnostic marker. The researchers suggest that future drugs or functional foods designed to inhibit REDD2 may help preserve β-cell health and combat the rising prevalence of diabetes.

Published in the Journal of Biological Chemistry, this study emphasizes the role of genetic factors in metabolic stress responses and offers hope for innovative interventions to address this growing health concern. For more details, visit source.