Paquot N, De Flines J, Rorive M
Service de Diabétologie, Nutrition et Maladies métaboliques, Département de Médecine, CHU de Liège, Belgique.
Rev Med Liege. 2012 May-Jun;67(5-6):332-6.
Obesity is explained by the joint actions of genetic susceptibility and environmental factors, such as a westernized lifestyle (sedentary lifestyle, calorie-dense foods), inducing an obesogenic environment. The search for obesity susceptibility genes remains complex, despite recent adavances made in the obesity genetics field. Except very rare monogenic type obesity, common obesity is thought to be polygenic and the genetic contribution to interindividual variation in common obesity has been estimated at 40-70 %. The genome-wide association studies have led to identify numerous genetic loci associated with body mass index and obesity risk. However, the predictive value of these loci to the obesity risk at the population level remains low. Finally, the influence of environmental factors on genetic susceptibility to weight gain is also related to epigenetic factors. Nutritional unbalance during fetal development may change the intrauterine environment and lead to altered gene expression (fetal programming) with alterations in DNA or histone methylation resulting in an increased susceptibility to chronic disease in adulthood, such as obesity.
肥胖是由遗传易感性和环境因素共同作用导致的，比如西化的生活方式（久坐不动的生活方式、高热量食物），从而营造出一种致胖环境。尽管肥胖遗传学领域最近取得了进展，但寻找肥胖易感基因仍然很复杂。除了非常罕见的单基因肥胖类型外，普通肥胖被认为是多基因的，遗传因素对普通肥胖个体间差异的贡献估计在40%至70%之间。全基因组关联研究已经确定了许多与体重指数和肥胖风险相关的基因位点。然而，这些位点在人群水平上对肥胖风险的预测价值仍然很低。最后，环境因素对体重增加遗传易感性的影响也与表观遗传因素有关。胎儿发育期间的营养失衡可能会改变子宫内环境，并导致基因表达改变（胎儿编程），DNA或组蛋白甲基化发生变化，从而增加成年后患慢性病的易感性，如肥胖。
