The human obesity gene map:: The 1999 update

被引:97
作者
Chagnon, YC [1 ]
Pérusse, L
Weisnagel, SJ
Rankinen, T
Bouchard, C
机构
[1] Univ Laval, Phys Act Sci Lab, Dept Social & Prevent Med, Div Kinesiol,Fac Med,PEPS, Ste Foy, PQ G1K 7P4, Canada
[2] Louisiana State Univ, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA
来源
OBESITY RESEARCH | 2000年 / 8卷 / 01期
关键词
obesity; linkages; QTL; genes; Mendelian syndrome;
D O I
10.1038/oby.2000.12
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
This report constitutes the sixth update of the human obesity gene map incorporating published results up to the end of October 1999, Evidence from the rodent and human obesity cases caused by single gene mutations, Mendelian disorders exhibiting obesity as a clinical feature, quantitative trait loci (QTL) uncovered in human genome-wide scans and in cross-breeding experiments with mouse, rat, pig and chicken models, association and linkage studies with candidate genes and other markers is reviewed. Twenty-five human cases of obesity can now be explained by variation in five genes, Twenty Mendelian disorders exhibiting obesity as one of their clinical manifestations have now been mapped. The number of different QTLs reported from animal models reaches now 98. Attempts to relate DNA sequence variation in specific genes to obesity phenotypes continue to grow, with 89 reports of positive associations pertaining to 40 candidate genes. Finally, 44 loci have linked to obesity indicators in genomic scans and other linkage study designs. The obesity gene map depicted in Figure 1 reveals that putative loci affecting obesity-related phenotypes can be found on all autosomes, with chromosomes 14 and 21 showing each one locus only. The number of genes, markers, and chromosomal regions that have been associated or linked with human obesity phenotypes continues to increase and is now well above 200.
引用
收藏
页码:89 / 117
页数:29
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