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L'obesite est une maladie complexe qui affecte pres d'une personne sur trois dans la plupart des pays industrialises. Les recherches menees au cours des dix dernieres annees dans les domaines de l'epidemiologie genetique et de la genetique moleculaire permettent d'affirmer que l'obesite, ainsi que la susceptibilite des individus a prendre ou a perdre du poids, sont en partie determinees par nos genes. Dans le cadre de l'etude des familles de Quebec, l'heritabilite des divers phenotypes de l'obesite varie de 10% a 50 % et les analyses de segregation suggerent qu'un (ou quelques) gene(s) a transmission autosomique recessive pourrai(en)t y exercer une influence majeure. La carte genetique de l'obesite, etablie a partir des resultats provenant d'etudes animales et humaines, indique que tous les chromosomes, a l'exception du chromosome Y, contiennent des genes ou des locus potentiellement impliques dans l'etiologie de cette maladie.
Physical Activity Sciences Laboratory Laval University Quebec, Canada (Bouchard) Department of Anthropology University of Texas Austin, Texas (Malina)
Knowledge and appreciation of the psychobiological mechanisms that influence body weight are critical to the understanding of obesity and the development of effective weight management interventions. However, these mechanisms are often not discussed in an integrative manner to examine how these factors interact to influence body weight and weight-related behaviors. A greater understanding of the biological determinants of weight-related behaviors and the etiology of obesity is therefore needed to improve quality of care for obese individuals and to develop effective strategies for prevention. The purpose of this symposium is to identify and discuss psychobiological influences on weight regulation including genetic influences, neural control of appetite, and the neurobiological basis of reward and behavior. These factors will be considered with respect to weight management interventions to provide an overview of best treatment practices and implications for behavior change strategies. This topic has relevance for all individuals who study or treat obesity, and this symposium will provide researchers and practitioners with valuable information regarding the biological basis for behaviors that influence body weight and the implications for weight management.
The role of the genotype in the response to short-term overfeeding was assessed by submitted six pairs of male monozygotic twins to a 4.2 MJ (1000 kcal) per day energy intake surplus for a period of 22 consecutive days. Individual differences in fat mass and fat-free mass gains were observed in response to overfeeding but they were not randomly distributed. Indeed, the within-pair resemblance in the response was striking when compared to the heterogeneity found among the pairs in adiposity and fat-free mass gains. The intrapair resemblance in the response to overfeeding as assessed by the intraclass coefficient computed with the individual changes, reached 0.88 for total fat mass and 0.76 for fat-free mass. A similar trend for a genetically determined pattern of adaptation to overfeeding was observed for resting metabolic rate (intraclass = 0.63), thermic effect of a meal (intraclass = 0.62), and energy cost of submaximal exercise (intraclass = 0.78) when the data were analysed in terms of changes in oxygen uptake. On the other hand, no major alterations in glucose and insulin response to a glucose load or a test meal, in cardio-pulmonary adaptation to submaximal exercise and in maximal exercise tolerance were found with overfeeding. In contrast, the response of suprailiac fat cell lipolysis (intraclass of about 0.7) and heparin releasable adipose tissue lipoprotein lipase (intraclass - 0.82) varied among individuals but was highly homogeneous within genotypes. Similarly, a genotype-overfeeding interaction effect was seen for serum triglycerides (intraclass = 0.69), HDL-cholesterol (intraclass = 0.85), and the HDL-cholesterol to total cholesterol ratio (intraclass = 0.82). Multiple correlation analyses suggest that much of the variance in the response of fat mass (R = 0.65) and fat-free mass (R = 0.81) is accounted for by alterations in the energy expenditure components assessed in the study. If one takes into account the measurement errors always present in such complex studies and the fact that only a limited fraction of the energy expenditure of activity was considered by design, one can conclude that the genotype determines to a large extent the response variation to short-term overfeeding. In particular, the genotype-overfeeding interaction effect for body composition changes seems to be mediated by the various energy expenditure components, themselves characterized by significant genotype-overfeeding interaction effects.(ABSTRACT TRUNCATED AT 400 WORDS)
No abstract is provided for this article.
L’obesite est devenue un probleme majeur de sante tres frequent dans les pays industrialises. Sa prevalence est en hausse constante. Meme les classes socio-economiques moyennes et aisees des pays en developpement n’y echappent pas. Elle presente un grand interet sur le plan medical parce qu’elle s’accompagne d’un plus grand risque d’anomalies metaboliques et de mortalite par diverses causes, en plus d’etre associee a des desordres psychologiques et de comportement chez une proportion importante de ceux et celles qui en sont affliges. On consacre maintenant des sommes enormes a la prevenir, a la traiter et a en contrer les comorbidites. La presente epidemie de surpoids et d’obesite que nous observons dans plusieurs pays hautement industrialises nous semble resulter principalement des diminutions importantes des depenses d’energie associees au travail physique et faisant suite au progres technique et a la mecanisation accrue des dernieres decennies. Neanmoins, nous avons maintenant de bonnes raisons de croire que certains individus sont plus susceptibles que d’autres d’avoir un bilan energetique positif pendant des periodes prolongees et d’accumuler une masse grasse croissante en presence d’un mode de vie sedentaire. Les travaux de l’epidemiologie genetique revelent que l’heritabilite de la masse corporelle ajustee pour la taille ou de la masse grasse atteint environ un tiers des differences individuelles observees dans la population en tenant compte de la variation associee a l’âge et au sexe. Il est possible que un ou quelques genes puissent jouer un role preponderant dans cette susceptibilite. Malheureusement, les travaux de la genetique moleculaire n’ont pas encore reussi a les mettre en evidence. Ils ont toutefois permis d’identifier plusieurs genes ou regions du genome caracterises par des liaisons genetiques significatives avec un ou des phenotypes de l’obesite. La recherche de ces genes de susceptibilite a l’obesite et des mutations qui en sont responsables est compliquee par le fait qu’il y a, de toute evidence, d’importantes interactions entre les genes et les determinants du bilan energetique.
