The overall aim of this study is to determine the degree to which isocaloric binge eating effects insulin levels; identify the mechanisms of the insulin response to binge eating, the impact of eating-induced changes in insulin on reproductive function, and the relative impact of insulin and androgen changes of lipid profile. Disordered eating behaviors, especially binge eating, are surprisingly prevalent in both obese older individuals and in non-obese young American women. Many of the risk factors for cardiovascular disease, including obesity, abdominal deposition of body fat, hyperinsulinemia, diabetes, hyperlipidemia, and hypertension, can be strongly influenced by the environment impact of eating behavior. The temporal pattern of eating has a significant impact on insulin metabolism in that more frequent small meals rapidly result inlower mean insulin levels than even three meals per day. Although hyperinsulinemia is typically associated with hyperlipidemia, other metabolic signals from the eating pattern may also influence lipid levels. For example, androgens are positively associated with elevated LDL cholesterol levels, and diet appears able to influence androgen levels by increasing or decreasing gonadotropin levels. The relationships between eating behavior, insulin levels, gonadotropin levels, and ovarian androgen secretion are critical to understanding the pathophysiology of Polycystic Ovary Syndrome (PCOS), in which affected women are oligomenorrheic and hyperandrogenic, as well as hyperinsulinemic. Other women are hyperinsulinemic compared to normal women, including obese women and pre-diabetic women, but their similarities and differences with women with PCIS have not been well delineated. To date, a primary genetic defect has been discerned in only a minority of these diagnostic subsets, so that functional defects of insulin resistance appear similar in obese, pre-diabetic, and PCOS women. These studies are designed for three major goals: 1) to determine the contribution of eating behavior to the expression of the PCOS phenotype, 2) to use binge eating-induced hyperinsulinemia as a experimental model to assess the effects of insulin on gonadotropin dynamics, ovarian androgen responsiveness, and subsequent lipid levels, and 3) to identify unique pathophysiologic mechanisms in women with PCOS compared to women who are simply obese or who are hyperinsulinemic because they are pre-diabetic.
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