Developmental Origins of Health and Disease Division, Institute of Developmental Sciences, University of Southampton School of Medicine, Southampton General Hospital, Southampton, UK.
J Nutr. 2010 Mar;140(3):648-52. doi: 10.3945/jn.109.111179. Epub 2010 Jan 27.
Metabolic syndrome (MetS) represents a combination of cardio-metabolic risk determinants, including central obesity, insulin resistance, glucose intolerance, dyslipidemia, hypertension, hyperinsulinemia, and microalbuminuria. The prevalence of MetS is rapidly increasing worldwide, largely as a consequence of the ongoing obesity epidemic. Environmental factors during periods early in development have been shown to influence the susceptibility to develop disease in later life. In particular, there is a wealth of evidence from both epidemiological and animal studies for greater incidence of features of MetS as a result of unbalanced maternal nutrition. The mechanisms by which nutritional insults during a period of developmental plasticity result in a MetS phenotype are now beginning to receive considerable scientific interest. This review focuses on recent data regarding these mechanisms, in particular the epigenetic and transcriptional regulation of key metabolic genes in response to nutritional stimuli that mediate persistent changes and an adult MetS phenotype. A continued and greater understanding of these mechanisms will eventually allow specific interventions, with a favorable impact on the global incidence of cardiovascular disease and type 2 diabetes in the future.
代谢综合征（MetS）代表了一系列心血管代谢危险因素的组合，包括中心性肥胖、胰岛素抵抗、葡萄糖耐量受损、血脂异常、高血压、高胰岛素血症和微量白蛋白尿。代谢综合征的患病率在全球范围内迅速增加，主要是由于肥胖症的持续流行。研究表明，在发育早期的环境因素会影响人在以后生活中患疾病的易感性。特别是，来自流行病学和动物研究的大量证据表明，由于母体营养失衡，代谢综合征的特征发生率更高。目前，人们对营养损伤在发育可塑性期间导致代谢综合征表型的机制开始产生浓厚的兴趣。这篇综述重点介绍了最近关于这些机制的研究数据，特别是关键代谢基因的表观遗传和转录调控，以响应营养刺激，介导持续变化和成年代谢综合征表型。对这些机制的进一步深入了解，最终将允许进行特定的干预，对未来全球心血管疾病和 2 型糖尿病的发病率产生有利影响。
