Genetics of human obesity

被引:41
作者
Boutin, P [1 ]
Froguel, P
机构
[1] Inst Pasteur, CNRS, Inst Biol Lille, F-59019 Lille, France
[2] Univ London Queen Mary & Westfield Coll, London E1 4NS, England
[3] St Bartholomews Hosp, London Genome Ctr, London, England
基金
英国医学研究理事会;
关键词
genetics; obesity; multifactorial disease; leptin; leptin receptor; POMC; MC4R; genome-wide scans; susceptibility genes for obesity; positional cloning; linkage studies; association studies; linkage disequilibrium;
D O I
10.1053/beem.2001.0153
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Obesity is a multifactorial condition. Environmental risk factors related to a sedentary lifestyle and unlimited access to food apply constant pressure in subjects with a genetic predisposition to gain weight. The fact that genetic defects can result in human obesity has been unequivocally established over the past 3 years with the identification of the genetic defects responsible for different monogenic forms of human obesity: the leptin, leptin receptor, pro-opiomelanocortin, pro-hormone convertase-1 and melanocortin-4 receptor genes. The common forms of obesity are, however, polygenic. The examination of specific genes for involvement in the susceptibility to common obesity has not yet yielded convincing results. Approaches involving the candidate genes and the positional cloning of major obesity-linked regions (state-of-the-art future prospects) will be discussed.
引用
收藏
页码:391 / 404
页数:14
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