Obesity is a public health epidemic that is commonly associated with insulin resistance, and predisposes people to development of Type II diabetes. I am interested in how insulin resistance affects nutrient metabolism, particularly in the post-prandial state, and the implications of this for obesity and diabetes. In the future, I intend to investigate effects of fasting and caloric restriction on post-prandial metabolism in lean, obese, and post-obese subjects.

Acute changes in insulin action, despite having different origins to chronic insulin resistance, can profoundly affect nutrient metabolism. For example, two days of fasting induces glucose intolerance following a normal mixed meal, and promotes non-hepatic decreased insulin action. The proposed study will investigate the effects of an acute change in insulin action induced by fasting, on post-prandial nutrient partitioning in lean and obese men and women. The relative oxidation rates of meal- derived lipid and carbohydrate will be determined in addition to storage of meal derived nutrients. It is hypothesized that glucose intolerance induced by fasting will be associated with a) greater post-prandial lipid oxidation (endogenous and meal-derived), and b) greater storage of meal derived carbohydrate as glycogen. As these data have direct implications for weight reduction practices, studies will be performed in both lean and obese, men and women.

F32DK059739

2001-07-01

1900-01-01