Abstract
During the past two decades, the prevalence of obesity has greatly risen worldwide. These changes have occurred among genetically stable populations, indicating that modifications of behavioral factors like dietary and physical activity must underlie the recent obesity epidemic. However, genetic factors undoubtedly have a great effect on individual predisposition, since 25 to 80 percent of the variation in body-mass index is heritable. Eating behavior, disordered eating behaviors and food preferences are in part heritable, and a family history of overeating is more frequent in obese individuals with binge-eating disorder than in the general population. The identification of genes causing both syndromic (Prader Willi) and rare monogenic (leptin / melanocortin pathways) forms of obesity, highlight the importance of genetic determinants in obesity. The common forms of obesity are, however, polygenic, and could modestly modulate behavior component. The recent identification of GAD2 gene variations modulating food intake and increasing the risk for severe obesity highlights the role of the GABA pathway in eating behavior. Other pathways involved in behavior, including Dopamine, serotonin and cannabinoid pathways are candidate for obese susceptibility genes. Modest individual effects of already identified at risk variants for abnormal food intake, may be amplified by gene-gene and geneenvironment interactions.
Keywords: melanocortin, GABA pathway, body-mass index, leptin
1