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Gene-Environment Interactions in Obesity

机译：肥胖症中的基因-环境相互作用

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Obesity is a global and growing problem. The detrimental health consequences of obesity are significant and include co-morbidities such as diabetes, cancer and coronary heart disease. The marked rise in obesity observed over the last three decades suggests that behavioural and environmental factors underpin the chronic mismatch between energy intake and energy expenditure. However, not all individuals become obese, suggesting that there is considerable variation in responsiveness to 'obesogenic'environments. Some individuals defend easily against a propensity to accumulate fat mass and become overweight whilst others are predisposed to gain weight, possibly as a function of genotype. The genetic contribution to obesity is well established. Common obesity is polygenic, involving complex gene-gene and gene-environment interactions, and it is these interactions that produce the multi-factorial obese phenotypes. Candidate gene variants for polygenic obesity appear to disrupt pathways involved in the regulation of energy intake and expenditure and include adrenergic receptors, uncoupling proteins, PPARG, POMC, MC4R and a set of single nucleotide polymorphisms in the FTO locus. Notably, the FTO gene is the most robust gene for common obesity characterised to date, and recent data shows that the FTO locus seems to confer risk of obesity through increasing energy intake and reduced satiety. Gene variants involved in pathways regulating addiction and reward behaviours may also play a role in predisposition to obesity. Understanding the routes through which the genotype is expressed will ultimately provide opportunities for developing strategies to intervene, as the interaction between genotype and environment is potentially modifiable through behaviour change.
机译：肥胖是一个全球性且日益严重的问题。肥胖对健康的有害影响是重大的，包括糖尿病，癌症和冠心病等合并症。在过去的三十年中观察到的肥胖显着上升表明，行为和环境因素是能量摄入和能量消耗之间长期不匹配的基础。但是，并非所有人都肥胖，这表明对“致肥胖”环境的反应能力存在很大差异。有些人很容易抵御积累脂肪和变得超重的倾向，而另一些人则倾向于增加体重，可能是基因型的作用。肥胖的遗传贡献已得到充分证实。普通肥胖是多基因的，涉及复杂的基因-基因和基因-环境相互作用，正是这些相互作用产生了多因素肥胖表型。多基因肥胖的候选基因变异似乎破坏了能量摄入和能量消耗的调节途径，包括肾上腺素能受体，解偶联蛋白，PPARG，POMC，MC4R和FTO基因座中的一组单核苷酸多态性。值得注意的是，FTO基因是迄今为止表征的最常见的肥胖症基因，最近的数据表明，FTO基因座似乎通过增加能量摄入和降低饱腹感而赋予了肥胖风险。参与调节成瘾和奖励行为途径的基因变异也可能在肥胖易感性中起作用。了解基因型表达的途径最终将为制定干预策略提供机会，因为基因型与环境之间的相互作用可能会通过行为改变而改变。

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