School of Biological Sciences, Institute of Developmental Sciences, University of Southampton, Southampton, UK.
Proc Nutr Soc. 2011 Feb;70(1):64-72. doi: 10.1017/S0029665110004027.
The rapid increase in the incidence of chronic non-communicable diseases over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environment also strongly influences the risk of developing such diseases in later life. Human studies have shown that low birth weight is associated with an increased risk of CVD, type II diabetes, obesity and hypertension, although recent studies have shown that over-nutrition in early life can also increase susceptibility to future metabolic disease. These findings have been replicated in a variety of animal models, which have shown that both maternal under- and over-nutrition can induce persistent changes in gene expression and metabolism within the offspring. The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. The demonstration of a role for altered epigenetic regulation of genes in the developmental induction of chronic diseases raises the possibility that nutritional or pharmaceutical interventions may be used to modify long-term cardio-metabolic disease risk and combat this rapid rise in chronic non-communicable diseases.
在过去的二十年中，慢性非传染性疾病的发病率迅速上升，这不能仅仅用遗传和成人生活方式因素来解释。现在有相当多的证据表明，胎儿和出生后早期的环境也强烈影响着以后生活中发生此类疾病的风险。人类研究表明，低出生体重与心血管疾病、2 型糖尿病、肥胖和高血压的风险增加有关，尽管最近的研究表明，生命早期的营养过剩也会增加对未来代谢性疾病的易感性。这些发现已经在各种动物模型中得到了复制，这些模型表明，母体营养不足和营养过剩都可以在后代中引起基因表达和代谢的持续变化。母体营养环境引起这些变化的机制开始被理解，并涉及特定基因的表观遗传调控的改变。基因表观遗传调控改变在发育过程中诱发慢性疾病的作用的证明提出了这样一种可能性，即营养或药物干预可能被用于改变长期的心脏代谢疾病风险，并对抗这种慢性非传染性疾病的迅速上升。
