Early Life Nutrition Research Unit, Academic Child Health, Division of Human Development, School of Clinical Sciences, University Hospital, Nottingham, UK.
Nat Rev Endocrinol. 2009 Nov;5(11):604-10. doi: 10.1038/nrendo.2009.195. Epub 2009 Sep 29.
The primary markers of the metabolic syndrome are central obesity, insulin resistance and hypertension. In this review, we consider the effect of changes in maternal nutrition during critical windows in fetal development on an individual's subsequent predisposition to the metabolic syndrome. The fetal origins of obesity, cardiovascular disease and insulin resistance have been investigated in a wide range of epidemiological and animal studies; these investigations highlight adaptations made by the nutritionally manipulated fetus that aim to maintain energy homeostasis to ensure survival. One consequence of such developmental plasticity may be a long term re-setting of cellular energy homeostasis, most probably via epigenetic modification of genes involved in a number of key regulatory pathways. For example, reduced maternal-fetal nutrition during early gestation to midgestation affects adipose tissue development and adiposity of the fetus by setting an increased number of adipocyte precursor cells. Importantly, clinically relevant adaptations to nutritional challenges in utero may only manifest as primary components of the metabolic syndrome if followed by a period of accelerated growth early in the postnatal period and/or if offspring become obese.
代谢综合征的主要标志物是中心性肥胖、胰岛素抵抗和高血压。在这篇综述中，我们考虑了在胎儿发育的关键窗口期母体营养变化对个体随后易患代谢综合征的影响。肥胖、心血管疾病和胰岛素抵抗的胎儿起源已经在广泛的流行病学和动物研究中得到了研究；这些研究强调了营养干预胎儿所做出的适应性改变，这些改变旨在维持能量平衡以确保生存。这种发育可塑性的一个后果可能是细胞能量平衡的长期重置，很可能是通过参与许多关键调节途径的基因的表观遗传修饰来实现。例如，孕早期至孕中期的母体-胎儿营养减少会通过增加脂肪细胞前体细胞的数量来影响胎儿的脂肪组织发育和肥胖。重要的是，如果随后在出生后的早期阶段经历了加速生长的时期，或者如果后代变得肥胖，那么与宫内营养挑战相关的临床相关适应性可能仅表现为代谢综合征的主要成分。
