UCD Institute of Food and Health, University College Dublin, Belfield, Dublin, Ireland.
Curr Opin Clin Nutr Metab Care. 2013 Jul;16(4):392-7. doi: 10.1097/MCO.0b013e3283620f45.
Research suggests that 65% of variation in obesity is genetic. However, much of the known genetic associations have little known function and their effect size small, thus the gene-environment interaction, including epigenetic influences on gene expression, is suggested to be an important factor in the susceptibilty to obesity. This review will explore the potential of epigenetic markers to influence expression of genes associated with obesity.
Epigenetic changes in utero are known to have direct implications on the phenotype of the offspring. More recently work has focused on how such epigenetic changes continue to regulate risk of obesity from infancy through to adulthood. Work has shown that, for example, hypomethylation of the MC4 gene causes an increase in expression, and has a direct impact on appetite and intake, and thus influences risk of obesity. Similar influences are also seen in other aspects of obesity including inflammation and adiposity.
Maternal diet during foetal development has many epigenetic implications, which affect the offspring's risk factors for obesity during childhood and adulthood, and even in subsequent generations. Genes associated with risk of obesity, are susceptible to epigenetic mutations, which have subsequent effects on disease mechanisms, such as appetite and impaired glucose and insulin tolerance.
研究表明，肥胖的 65%是由遗传决定的。然而，许多已知的遗传相关性的功能知之甚少，其效应大小也很小，因此基因-环境相互作用，包括对基因表达的表观遗传影响，被认为是肥胖易感性的一个重要因素。这篇综述将探讨表观遗传标记对与肥胖相关基因表达的影响。
子宫内的表观遗传变化已知对后代的表型有直接影响。最近的研究工作集中在这些表观遗传变化如何继续调节从婴儿期到成年期肥胖的风险。研究表明，例如，MC4 基因的低甲基化导致表达增加，直接影响食欲和摄入量，从而影响肥胖的风险。在肥胖的其他方面，如炎症和肥胖，也存在类似的影响。
胎儿发育过程中母体的饮食有许多表观遗传意义，这会影响儿童期和成年期肥胖的后代风险因素，甚至在后代中也是如此。与肥胖风险相关的基因易受表观遗传突变的影响，这些突变随后对疾病机制产生影响，如食欲和葡萄糖及胰岛素耐量受损。
