title: [Genetics of human obesity].
abstract: BACKGROUND
  Both genetic and environmental aspects are recognized in the obesity field but we are not able to elucidate multiple genes and gene-environment interactions with the present resources and tools used in the study of this complex disease. The purpose of this paper is to present some examples of the knowledge acquired in the field of obesity genetics and the new ongoing tools and developments that aim at studying the contribution of genes to obesity and their response to environmental changes.
  
  
  RESULTS
  In rare cases of monogenic obesities, genetic tools have proved extremely powerful for identifying the genes responsible and for defining new syndromes. However, in common obesity, most studies include the search for genotype-phenotype associations without taking into account the influence of environment (diet, sedentary lifestyle) in the relationship. Among the limitations to this integrated approach, one can cite the difficulty of having large enough samples as well as biocomputing tools that are still in their infancy for accessing the question of multiple interactions with no "a priori hypotheses". This picture will probably change rapidly in the future.
  
  
  CONCLUSIONS
  Large databases and DNA and biological sample banks will be available with updated environmental information and precise phenotypes thanks especially to European working groups. The capacity for studying multiple genes at once at the DNA or RNA levels is rapidly growing. Finally, tremendous progress in biocomputing will allow the integration of information from different sources (i.e. environment, phenotype, genotype, gene expression) and thus improve our ability to deal with complexity.
authors.affiliation: Inserm Avenir, Paris EA3502, université Pierre-et-Marie-Curie, Paris VI, France.
authors.forename: C
authors.initials: C
authors.lastname: Lubrano-Berthelier
authors.forename: K
authors.initials: K
authors.lastname: Clément
mesh_terms: D000328:Adult; D000818:Animals; D002648:Child; D015331:Cohort Studies; D004195:Disease Models, Animal; D004777:Environment; D005260:Female; D005544:Forecasting; D015870:Gene Expression; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006706:Homeostasis; D006801:Humans; D007223:Infant; D020738:Leptin / Q000097:blood / Q000235:genetics / Q000627:therapeutic use; D008297:Male; D051379:Mice; D009154:Mutation; D009765:Obesity / Q000188:drug therapy / Q000209:etiology / Q000235:genetics* / Q000378:metabolism / Q000517:prevention & control; D010641:Phenotype; D011110:Polymorphism, Genetic; D044105:Receptor, Melanocortin, Type 4 / Q000235:genetics; D011956:Receptors, Cell Surface / Q000235:genetics; D054411:Receptors, Leptin; D012306:Risk; D013577:Syndrome
chemical_list: D020738:Leptin; D044105:Receptor, Melanocortin, Type 4; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin