Obesity has become one of the major health crises facing the United States and many other nations. It is linked to a host of serious health issues, including type 2 diabetes. Although obesity is often dismissed as an issue of willpower and addressed through behavioral modification (decreased consumption and increased physical activity), basic science research at UCSF and elsewhere has revealed that genetics play a tremendous role in predisposing individuals to obesity.
When individuals become overweight, their fat cells (adipocytes) fill up with dietary fat, something that we now know induces the cells’ death. When the body’s scavengers of dead cells (macrophages) dispose of these adipocytes, they are exposed to extremely high levels of the fats that were previously stored inertly within the adipocytes. This exposure causes macrophages to become inflamed and stimulate the secretion of immune factors called cytokines. Over time these cytokines contribute to insulin resistance and diabetes, as well as other conditions such as heart disease.
Our research team includes world specialists in the areas of obesity, metabolism, and the related conditions of inflammation and insulin resistance. This team’s work centers on gaining a better understanding of:
- Genetic variations responsible for obesity
- How obesity can alter molecular pathways of insulin utilization
- The mechanisms by which the function of inflammatory cells can be negatively altered by dietary fats
- How the brain regulates body weight, energy stores, and glucose levels
- The factors that regulate how and when fat cells release stored fat