Genetics of human obesity.
Obesity is a multifactorial condition. Environmental risk factors related to a sedentary life-style 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.
Boutin
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CNRS-Institute of Biology of Lille, Pasteur Institute of Lille, France.
Froguel
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P
D016282:Aspartic Acid Endopeptidases / Q000235:genetics; D002352:Carrier Proteins / Q000235:genetics; D008040:Genetic Linkage; D006801:Humans; D020738:Leptin / Q000235:genetics; D009765:Obesity / Q000453:epidemiology / Q000235:genetics*; D011333:Pro-Opiomelanocortin / Q000235:genetics; D043484:Proprotein Convertases; D044105:Receptor, Melanocortin, Type 4; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D018000:Receptors, Peptide / Q000235:genetics
D002352:Carrier Proteins; D020738:Leptin; D044105:Receptor, Melanocortin, Type 4; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D018000:Receptors, Peptide; D011333:Pro-Opiomelanocortin; D043484:Proprotein Convertases; D016282:Aspartic Acid Endopeptidases