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，中间值 密度脂蛋白胆固醇，极低密度脂蛋白 胆固醇(VLDL-C)和脂蛋白(A)，或Lp(A)，并呈负 与高密度脂蛋白胆固醇(HDL-C)水平有关。 最近的研究集中在胰岛素抵抗在 冠心病的建立。事实证明， 膳食胆固醇提高血浆胆固醇浓度的能力 患有混合性高脂血症(胆固醇升高和 甘油三酯)比那些有其他脂类表型的人更高。 混合性高脂血症患者通常表现为一群 会增加患冠心病风险的异常。这些 异常包括空腹甘油三酯升高和高血糖降低 密度(高密度脂蛋白)脂蛋白浓度，增强程度 餐后血脂，低密度脂蛋白(低密度脂蛋白)更小和更稠密- 颗粒、高尿酸血症、高血压和高胰岛素血症。基于 我们的实验室观察到患有混合性高脂血症的受试者 对饮食中的胆固醇表现出更大的反应，有极好的 患有胰岛素抵抗(或其子集)的受试者 代表了一大部分拥有 对饮食中的胆固醇反应过度。为了测试这一点 假设胰岛素新陈代谢的差异可以解释 膳食胆固醇升高血浆能力的变异性 胆固醇，有必要选择一个人群，这些研究 应该被执行。在此背景下，选择了绝经后妇女 作为我们的代表性子集。它们构成了一个庞大的、快速增长的 我们人口中的一部分，总体健康，非肥胖，非糖尿病 胰岛素在体内的作用范围广泛。我们的目标是 研究将证明对血糖、胰岛素和 饮食中胆固醇摄入量变化的脂蛋白代谢是 定义为胰岛素的绝经后妇女显著升高 抵抗的与胰岛素敏感的相比。

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.