The human obesity gene map:: The 2000 update

被引:66
作者
Pérusse, L
Chagnon, YC
Weisnagel, SJ
Rankinen, T
Snyder, E
Sands, J
Bouchard, C
机构
[1] Univ Laval, Dept Social & Prevent Med, Div Kinesiol, Fac Med, Ste Foy, PQ G1K 7P4, Canada
[2] Louisiana State Univ, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA
来源
OBESITY RESEARCH | 2001年 / 9卷 / 02期
关键词
association; linkages; QTL; genes; Mendelian syndrome;
D O I
10.1038/oby.2001.17
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
This report constitutes the seventh update of the human obesity gene map incorporating published results up to the end of October 2000. Evidence from the rodent and human obesity cases caused by single-gene mutations, Mendelian disorders exhibiting obesity as a clinical feature, quantitative trait loci uncovered in human genome-wide scans and in cross-breeding experiments in various animal models, and association and linkage studies with candidate genes and other markers are reviewed. Forty-seven human cases of obesity caused by single-gene mutations in six different genes have been reported in the literature to date. Twenty-four Mendelian disorders exhibiting obesity as one of their clinical manifestations have now been mapped. The number of different quantitative trait loci reported from animal models currently reaches 115. Attempts to relate DNA sequence variation in specific genes to obesity phenotypes continue to grow, with 130 studies reporting positive associations with 48 candidate genes. Finally, 59 loci have been linked to obesity indicators in genomic scans and other linkage study designs. The obesity gene map reveals that putative loci affecting obesity-related phenotypes can be found on all chromosomes except chromosome Y. A total of 54 new loci have been added to the map in the past 12 months and the number of genes, markers, and chromosomal regions that have been associated or linked with human obesity phenotypes is now above 250. Likewise, the number of negative studies, which are only partially reviewed here, is also on the rise.
引用
收藏
页码:135 / 169
页数:35
相关论文
共 370 条
[1]   Association of polymorphisms at the SR-BI gene locus with plasma lipid levels and body mass index in a white population [J].
Acton, S ;
Osgood, D ;
Donoghue, M ;
Corella, D ;
Pocovi, M ;
Cenarro, A ;
Mozas, P ;
Keilty, J ;
Squazzo, S ;
Woolf, EA ;
Ordovas, JM .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1999, 19 (07) :1734-1743
[2]   Linkage mapping of a new syndromic form of X-linked mental retardation, MRXS7, associated with obesity [J].
Ahmad, W ;
De Fusco, M ;
ul Haque, MF ;
Aridon, P ;
Sarno, T ;
Sohail, M ;
ul Haque, S ;
Ahmad, M ;
Ballabio, A ;
Franco, B ;
Casari, G .
EUROPEAN JOURNAL OF HUMAN GENETICS, 1999, 7 (07) :828-832
[3]   Mutation analysis of two Japanese patients with Fanconi-Bickel syndrome [J].
Akagi, M ;
Inui, K ;
Nakajima, S ;
Shima, M ;
Nishigaki, T ;
Muramatsu, T ;
Kokubu, C ;
Tsukamoto, H ;
Sakai, N ;
Okada, S .
JOURNAL OF HUMAN GENETICS, 2000, 45 (01) :60-62
[4]  
Aldred MA, 2000, HUM MUTAT, V16, P183, DOI 10.1002/1098-1004(200009)16:3<183::AID-HUMU1>3.0.CO
[5]  
2-L
[6]   Study of the Trp64Arg Polymorphism of the β3-adrenergic receptor in Greek women with gestational diabetes [J].
Alevizaki, M ;
Thalassinou, L ;
Grigorakis, SI ;
Philippou, G ;
Lili, K ;
Souvatzoglou, A ;
Anastasiou, E .
DIABETES CARE, 2000, 23 (08) :1079-1083
[7]  
Anderson JL, 1999, AM J MED GENET, V82, P161, DOI 10.1002/(SICI)1096-8628(19990115)82:2<161::AID-AJMG12>3.0.CO
[8]  
2-0
[9]   GENETIC-MAPPING OF QUANTITATIVE TRAIT LOCI FOR GROWTH AND FATNESS IN PIGS [J].
ANDERSSON, L ;
HALEY, CS ;
ELLEGREN, H ;
KNOTT, SA ;
JOHANSSON, M ;
ANDERSSON, K ;
ANDERSSONEKLUND, L ;
EDFORSLILJA, I ;
FREDHOLM, M ;
HANSSON, I ;
HAKANSSON, J ;
LUNDSTROM, K .
SCIENCE, 1994, 263 (5154) :1771-1774
[10]  
Arcuri P, 2000, INT J MOL MED, V6, P97