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GENETIC EPIDEMIOLOGY OF SEX HORMONES AND LIPOPROTEINS

性激素和脂蛋白的遗传流行病学

基本信息

批准号：
3315311
负责人：
DENNIS L SPRECHER
金额：
$ 27.14万
依托单位：
UNIVERSITY OF CINCINNATI
依托单位国家：
美国
项目类别：
财政年份：
1984
资助国家：
美国
起止时间：
1984-09-01 至 1994-04-30
项目状态：
已结题

项目摘要

An extension and expansion of the study Sex Hormones and Lipoproteins in Adolescent Males (RO1-HD-18281) to include all first degree relative and the oldest paternal uncle or aunt of a random subset of the white male student and the offspring of early CHD patient populations is proposed to assess: 1) the contribution of sex steroid hormones to the risk profiles of adult men beyond the traditional CHD risk factors; 2) the risk of developing CHD at an individual level in the adolescent population using fitted logistic models; 3) the nature of family resemblance for such risk estimates; and 4) the relative contributions of genetics and shared household environments to the familial associations, singly and jointly, of sex steroid hormones, lipids, lipoprotein cholesterols, apolipoproteins, blood pressure and ponderosity. Thus, this study will provide unique insights into the genetic basis of the joint associations of sex steroid hormones and traditional CHD risk factors. Specifically, we will quantitate total and free testosterone (T), estradiol (E2), testosterone- estrogen binding globulin (TEBG), dehydroepiandrosterone sulfate (DHEAS), total, HDL and LDL cholesterol, triglycerides, HDL2 and HDL3 subfractions, apolipoproteins A1, A2, B (and determine E isoforms), height, weight, skinfolds and diet on 200 white male students, 100 offspring approximately 1050 first degree relatives, and 300 paternal uncles or aunts. We will obtain these measures on two occasions one year apart. Preliminary data from our current study (HD 18281) indicate that the offspring have 1) sex steroid hormone profiles which differ from those of the (healthy) school-based subjects; 2) greater mean levels of total cholesterol, low density lipoprotein cholesterol, and apolipoprotein B than the school-based subjects; and 3) that reductions in adolescent male HDL2 precede the decrease in total HDL-C. We will conduct these studies in the families of the same white school students and offspring with whom we have been working successfully (greater than or equal to 93% retention rate at the end of Visit 5) for the past 21/2 years. The proposed research is expected to improve significantly our knowledge of CHD risk, of the familial associations and interactions of coronary risk factors including sex steroid hormones and lipids. Thus, this study should indicate possible areas for intervention.

性激素和生殖激素研究的延伸和扩展青少年男性中的脂蛋白（RO 1-HD-18281），包括所有一级亲属和最年长的叔叔或阿姨白色男性学生和后代的随机子集建议对早期CHD患者人群进行评估：1）性类固醇激素对成年人患病风险的影响男性超越传统的冠心病危险因素; 2）在青少年人群中发生个体水平的CHD 使用拟合logistic模型; 3）家族相似性的性质对于这种风险估计;和4）的相对贡献遗传学和共同的家庭环境，性类固醇激素，脂质，脂蛋白胆固醇、载脂蛋白、血压和笨重因此，这项研究将提供独特的见解，性类固醇激素联合作用的遗传基础，传统CHD危险因素。具体来说，我们将量化总睾酮和游离睾酮（T）、雌二醇（E2）、睾酮- 硫酸脱氢表雄酮（DHEAS）、总、HDL和LDL胆固醇、甘油三酯、HDL 2 和HDL 3亚组分、载脂蛋白A1、A2、B（并测定 200名白色男性的E亚型）、身高、体重、皮褶厚度和饮食学生，100个后代大约1050个一级亲属，还有300个叔叔阿姨我们将采取这些措施一年内有两次我们的初步数据显示，目前的研究（HD 18281）表明，后代有1）性别类固醇激素的配置文件，不同于那些（健康）以学校为基础的受试者; 2）总胆固醇的平均水平更高，低密度脂蛋白胆固醇和载脂蛋白B 学校为基础的科目;和3）减少青少年男性 HDL 2先于总HDL-C下降。我们会进行这些研究在同一所白色学校的学生的家庭中进行，和我们成功合作的后代（访视5结束时留存率≥ 93%）在过去的两年半里。预计拟议的研究将显著提高我们对冠心病风险的认识，冠状动脉危险因素的关联和相互作用，性类固醇激素和脂质。因此，这项研究表明，可能的干预领域。