Genes involved in animal models of obesity and anorexia.
Pathological deviations in bodyweight is a major increasing health problem in industrialized societies. It is currently unclear what genetic mechanisms are involved in the long-term control of human body-weight and to what extent these genes are involved in pathological deviations of bodyweight control such as anorexia and obesity. Major support for the concept of genetic control of bodyweight has recently emerged from different animal models. A number of new genes have been found during recent years that, when mutated, have a negative effect on bodyweight in animals and sometimes also in man. Although available evidence points toward a multifactorial nature of weight disorders in most human subjects, the single genes isolated in animal models may become powerful tools to elucidate the genetics also in man. In addition, these genes may serve to promote the development of targeted small-drug pharmaceuticals aimed at novel biochemical pathways. Finally, the uncovering of several quantitative trait loci (QTL) influencing body mass, body fat or fat topography in the mouse and rat has now also made it possible to perform studies of polygenically caused obesity in rodents. The role of the Genome Project in developing a complete gene map will greatly facilitate transforming these OTLs to actual molecules involved in the biology of bodyweight.
Schalling
M
M
Neurogenetics Unit, Center for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden. martin.schalling@cmm.ki.se
Johansen
J
J
Nordfors
L
L
Lönnqvist
F
F
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D000855:Anorexia / Q000235:genetics*; D004195:Disease Models, Animal; D006801:Humans; D007333:Insulin Resistance; D020738:Leptin; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics*; D009154:Mutation; D009765:Obesity / Q000235:genetics*; D011506:Proteins / Q000235:genetics*; D051381:Rats
D020738:Leptin; D011506:Proteins