METABOLIC AND GENETIC MARKERS FOR DIETARY OBESITY

饮食性肥胖的代谢和遗传标志物

• 批准号: 2145127
• 负责人: David Brian West
• 金额: $ 17.54万
• 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/2145127
• 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.

肥胖是许多疾病的一个严重的独立危险因素