One probable cause of obesity’s health consequences is the body’s inability to expand fat tissues by increasing the number of adipocytes (fat cells). This lack of new adipocytes causes existing adipocytes to grow larger and leak fatty acids and inflammatory molecules into the bloodstream, resulting in insulin resistance and type 2 diabetes. The regulatory mechanisms that control the number of adipocytes remain unclear.

Fajun Yang, Ph.D., and colleagues have found that a protein called Cyclin C (CCNC), plays a major role in fat cell development and metabolism. Using mouse models, the researchers have shown that reducing CCNC activity led to healthier fat remodeling, smaller fat cells, less insulin resistance, and in some cases a “metabolically healthy obesity” state. The National Institutes of Health has awarded Dr. Yang a five-year, $3.2 million grant to explore how CCNC influences fat remodeling under different conditions, such as high-fat diets and cold exposure. His team will study how fat tissue responds when CCNC is missing and will investigate how the liver communicates with fat tissue through CCNC and the liver protein PDGF-AA. By uncovering how CCNC controls healthy versus unhealthy fat growth, this research could lead to new approaches for preventing or treating obesity and diabetes.

Dr. Yang is professor of medicine and of developmental & molecular biology at Einstein. (1R01DK139610-01A1)