METABOLIC AND GENETIC MARKERS FOR DIETARY OBESITY

饮食性肥胖的代谢和遗传标志物

• 批准号: 2145129
• 负责人: David Brian West
• 金额: $ 18.24万
• 依托单位: LSU PENNINGTON BIOMEDICAL RESEARCH CTR
• 依托单位国家: 美国
• 财政年份: 1994
• 资助国家: 美国
• 起止时间: 1994-09-15 至 1997-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2145129
• 关键词: adipose tissue; animal breeding; animal genetic material tag; animal population genetics; body weight; computer assisted sequence analysis; dietary lipid; gene expression; genetic markers; genetic models; genetic strain; genotype; hormone receptor; laboratory mouse; linkage mapping; lipolysis; northern blottings; nutrition related tag; obesity; phenotype; polymerase chain reaction; receptor binding; restriction fragment length polymorphism; somatotropin; southern blotting

Obesity is a serious independent risk factor for a number of disorders including diabetes, hypertension and cardiovascular disease. Development of effective measures to treat or prevent obesity will have a significant impact upon the incidence of these other diseases. Obesity is caused by a number of factors. There is a significant genetic component affecting the risk for the development of obesity and environmental factors such as dietary fat content also influence its expression. Interactions of predisposing genes with dietary fat may also be very important in determining the risk for obesity in an individual. The long-term goal of this project is to identify and characterize the genes which predispose for the development of obesity. We propose to use a mouse model initially to identify these genes and then to determine if the same genes or metabolic pathways are controlling the expression of human obesity. The overall approach which we propose to take is the mapping of quantitative trait loci (QTLs) in mouse populations segregating for sensitivity to dietary obesity. In this application, the specific aims are to: A. complete a linkage map of the loci controlling differential sensitivity to dietary obesity in the AKR/J x SWR/J mouse model. B. evaluate the role of specific genetic loci linked to dietary obesity in the AKR/J x SWR/J model in several other genetic models of dietary obesity. C. develop congenic strains for each locus, and several combinations of loci, in order to determine their relative quantitative contribution to the phenotype of dietary obesity. D. evaluate the role of specific candidate genes at these loci.

肥胖是一个严重的独立的危险因素， 包括糖尿病、高血压和心血管疾病。 发展 有效的治疗或预防肥胖的措施将有显着的 对其他疾病的影响。 肥胖是由以下原因引起的： 一系列因素。有一个重要的遗传因素影响着 肥胖和环境因素的发展风险，如 膳食脂肪含量也影响其表达。 相互作用 饮食中脂肪的易感基因也可能非常重要， 确定个体肥胖的风险。 的长期目标 这个项目是为了识别和描述基因， 肥胖症的发展。 我们建议最初使用小鼠模型 来识别这些基因，然后确定是否有相同的基因或 代谢途径控制着人类肥胖症的表达。 的 我们建议采取的总体方法是绘制定量的 在分离的小鼠群体中， 饮食性肥胖 在本申请中，具体目标是： A.完成控制差异敏感性的基因座的连锁图 AKR/J x SWR/J小鼠模型中的饮食性肥胖。 B。评估与饮食性肥胖相关的特定遗传位点在以下方面的作用： AKR/J × SWR/J模型在其他几种膳食遗传模型中 肥胖 C.为每个基因座开发同类菌株，以及 基因座，以确定其相对数量的贡献， 饮食性肥胖的表型。 D.评估这些位点上特定候选基因的作用。