HORMONAL AND METABOLIC IMPACT OF BINGE EATING IN WOMEN

这项研究的总体目标是确定等卡路里暴食对胰岛素水平的影响程度；确定暴饮暴食引起的胰岛素反应的机制；饮食诱导的胰岛素变化对生殖功能的影响；以及胰岛素和雄激素变化对血脂谱的相对影响。饮食失调行为，尤其是暴饮暴食，在肥胖的老年人和非肥胖的年轻美国女性中都令人惊讶地普遍存在。许多心血管疾病的危险因素，包括肥胖、腹部脂肪沉积、高胰岛素血症、糖尿病、高脂血症和高血压，都会受到饮食行为环境影响的强烈影响。饮食的时间模式对胰岛素代谢有重大影响，因为更频繁的小餐很快会导致平均胰岛素水平比一天三餐更低。虽然高胰岛素血症通常与高脂血症有关，但来自饮食模式的其他代谢信号也可能影响血脂水平。例如，雄激素与升高的低密度脂蛋白水平呈正相关，饮食似乎能够通过增加或降低促性腺激素水平来影响雄激素水平。进食行为、胰岛素水平、促性腺激素水平和卵巢雄激素分泌之间的关系对于了解多囊卵巢综合征(PCOS)的病理生理学至关重要。在PCOS中，受影响的妇女有月经过少、高雄激素分泌和高胰岛素血症。其他女性与正常女性相比存在高胰岛素血症，包括肥胖女性和糖尿病前期女性，但他们与多囊卵巢综合征女性的异同还没有很好地描绘出来。到目前为止，在这些诊断亚群中只有一小部分发现了原发基因缺陷，因此在肥胖、糖尿病前期和多囊卵巢综合征女性中，胰岛素抵抗的功能缺陷看起来类似。这些研究旨在达到三个主要目标：1)确定饮食行为对PCOS表型表达的贡献；2)以暴饮暴食诱导的高胰岛素血症为实验模型，评估胰岛素对促性腺激素动态、卵巢雄激素反应性及随后的血脂水平的影响；3)确定与单纯肥胖或因糖尿病前期而高胰岛素血症患者相比，PCOS女性独特的病理生理机制。

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 PCOS 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.