The Human Obesity Gene Map: The 1999 Update

Authors

  • Yvon C. Chagnon PhD,

    Corresponding author
    1. Physical Activity Sciences Laboratory, Division of Kinesiology, Department of Social and Preventive Medicine, Faculty of Medicine, Laval University, Sainte-Foy, Québec, Canada, G1K 7P4; and the
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  • Louis Pérusse,

    1. Physical Activity Sciences Laboratory, Division of Kinesiology, Department of Social and Preventive Medicine, Faculty of Medicine, Laval University, Sainte-Foy, Québec, Canada, G1K 7P4; and the
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  • S. John Weisnagel,

    1. Physical Activity Sciences Laboratory, Division of Kinesiology, Department of Social and Preventive Medicine, Faculty of Medicine, Laval University, Sainte-Foy, Québec, Canada, G1K 7P4; and the
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  • Tuomo Rankinen,

    1. Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana, LA 70808
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  • Claude Bouchard

    1. Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana, LA 70808
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Physical Activity Sciences Laboratory, Division of Kinesiology, Department of Social and Preventive Medicine, Faculty of Medicine, PEPS, Laval University, Ste-Foy, Québec G1K 7P4, Canada. E-Mail: Yvon.Chagnon@kin.msp.ulaval.ca

Abstract

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 crossbreeding 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.

Figure 1.

Figure 1.

The 1999 human obesity gene map. The map includes all putative obesity-related phenotypes identified from the various lines of evidence reviewed in the article. The chromosomes and their regions are from the Gene Map of the Human Genome web site hosted by the National Center for Biotechnology Information, National Institutes of Health, Bethesda, MD (URL:http:www.ncbi.nlm.nih.gov). The chromosome number and the size of each chromosome in megabases (Mb) are given at the top and bottom of the chromosomes, respectively. Loci abbreviations and full names are given in the Appendix. The abbreviations for QTLs are given in Table 4.

Figure 1.

Figure 1.

The 1999 human obesity gene map. The map includes all putative obesity-related phenotypes identified from the various lines of evidence reviewed in the article. The chromosomes and their regions are from the Gene Map of the Human Genome web site hosted by the National Center for Biotechnology Information, National Institutes of Health, Bethesda, MD (URL:http:www.ncbi.nlm.nih.gov). The chromosome number and the size of each chromosome in megabases (Mb) are given at the top and bottom of the chromosomes, respectively. Loci abbreviations and full names are given in the Appendix. The abbreviations for QTLs are given in Table 4.

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