The genetic contribution to non-syndromic human obesity

被引:260
作者
Walley, Andrew J. [1 ]
Asher, Julian E. [1 ]
Froguel, Philippe [1 ,2 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Sect Genom Med, London W12 0NN, England
[2] Inst Pasteur, Inst Biol, CNRS8090, F-59019 Lille, France
基金
英国惠康基金; 英国医学研究理事会;
关键词
GENOME-WIDE ASSOCIATION; BODY-MASS INDEX; LEPTIN RECEPTOR GENE; BROWN ADIPOSE-TISSUE; COPY NUMBER VARIATION; EARLY-ONSET OBESITY; SINGLE-NUCLEOTIDE POLYMORPHISMS; FTO GENE; MELANOCORTIN-4; RECEPTOR; SEQUENCE VARIANTS;
D O I
10.1038/nrg2594
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The last few years have seen major advances in common non-syndromic obesity research, much of it the result of genetic studies. This Review outlines the competing hypotheses about the mechanisms underlying the genetic and physiological basis of obesity, and then examines the recent explosion of genetic association studies that have yielded insights into obesity, both at the candidate gene level and the genome-wide level. With obesity genetics now entering the post-genome-wide association scan era, the obvious question is how to improve the results obtained so far using single nucleotide polymorphism markers and how to move successfully into the other areas of genomic variation that may be associated with common obesity.
引用
收藏
页码:431 / 442
页数:12
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