METABOLIC RESPONSES TO VARIATION IN DIETARY COMPOSITION

动脉粥样硬化性冠状动脉疾病（CAD）与 低密度脂蛋白胆固醇（LDL-C）水平，中间 密度脂蛋白胆固醇（IDL-C），极低密度脂蛋白 胆固醇（VLDL-C）和脂蛋白（a），或Lp（a），并呈阴性 与高密度脂蛋白胆固醇（HDL-C）水平相关。 最近的研究集中在胰岛素抵抗在 冠心病的发病。 已显示 膳食胆固醇升高血浆胆固醇浓度的能力 在患有混合型高脂血症（胆固醇增加， 甘油三酸酯）大于那些谁拥有其他脂质表型。 患有混合型高脂血症的个体通常表现为一簇高脂血症。 这些异常会增加冠心病的风险。 这些 异常包括较高的空腹甘油三酯和较低的高甘油三酯。 高密度脂蛋白（HDL）脂蛋白浓度， 餐后脂血症，小而致密的低密度脂蛋白（LDL）- 颗粒、高尿酸血症、高血压和高胰岛素血症。基于 我们的实验室观察发现， 显示出对饮食胆固醇的更大反应， 胰岛素抵抗受试者（或其子集） 代表了人口中很大一部分， 对饮食胆固醇的反应过度。 为了测试这个 假设胰岛素代谢的差异解释了 饮食胆固醇升高血浆胆固醇水平的能力的变异性 胆固醇，有必要选择一个人群，其中这些研究 应该执行。 在此背景下，选择绝经后妇女 作为我们的代表子集。 它们构成了一个庞大而迅速增长的 我们的一部分健康的非肥胖、非糖尿病人群 个体在体内胰岛素作用的广泛范围内。 我们的目标 研究将证明对葡萄糖、胰岛素和 脂蛋白代谢的变化，饮食胆固醇摄入量是 在绝经后妇女中显著增强，定义为胰岛素 胰岛素抵抗与胰岛素敏感相比。

Atherosclerotic coronary artery disease (CAD) is positively asociated with levels of low density lipoprotein cholesterol (LDL-C), imtermediate density lipoprotein cholesterol (IDL-C), very low density lipoprotein cholesterol (VLDL-C), and lipoprotein (a), or Lp(a), and is negatively associated with levels of high density lipoprotein cholesterol (HDL-C). Recently research has focused on the role that insulin resistance plays in the establishment of coronary heart disease. It has been shown that the ability of dietary cholesterol to raise plasma cholesterol concentration in individuals with combined hyperlipidemia (increased cholesterol and triglycerides) is greater than those who have other lipid phenotypes. Individuals with combined hyperlipidemia often present with a cluster of abnormalities which increase the risk of coronary heart disease. These abnormalities consist of higher fasting triglyceride and lower high density (HDL) lipoprotein concentrations, an enhanced degree of postprandial lipemia, smaller and denser low density lipoprotein (LDL)- particles, hyperuricemia, hypertension and hyperinsulinemia. Based upon our laboratory observations that subjects with combined hyperlipidemia show a greater response to dietary cholesterol, there is an excellent chance that subjects with insulin resistance (or a subset thereof) represent a significant fraction of the population that have an exaggerated response to dietary cholesterol. In an effort to test this hypothesis that differences in insulin metabolism account for the variability in the ability of dietary cholesterol to raise plasma cholesterol, it is necessary to select a population in which these studies should be performed. In this context, postmenopausal women were selected as our representative subset. They comprise a large and rapidly growing segment of our population of generally healthy non-obese, non-diabetic individuals over a wide range of in vivo insulin action. The goal of our study will be to prove that the untoward effects on glucose, insulin, and lipoprotein metabolism of variations in dietary cholesterol intake are significantly acentuated in postmenopausal women defined as being insulin resistant as compared to insulin sensitive.