Mark H Vickers, Liggins Institute and the National Research Centre for Growth and Development, University of Auckland, Auckland 1023, New Zealand.
World J Diabetes. 2011 Sep 15;2(9):137-48. doi: 10.4239/wjd.v2.i9.137.
Metabolic disease results from a complex interaction of many factors, including genetic, physiological, behavioral and environmental influences. The recent rate at which these diseases have increased suggests that environmental and behavioral influences, rather than genetic causes, are fuelling the present epidemic. In this context, the developmental origins of health and disease hypothesis has highlighted the link between the periconceptual, fetal and early infant phases of life and the subsequent development of adult obesity and the metabolic syndrome. Although the mechanisms are yet to be fully elucidated, this programming was generally considered an irreversible change in developmental trajectory. Recent work in animal models suggests that developmental programming of metabolic disorders is potentially reversible by nutritional or targeted therapeutic interventions during the period of developmental plasticity. This review will discuss critical windows of developmental plasticity and possible avenues to ameliorate the development of postnatal metabolic disorders following an adverse early life environment.
代谢性疾病是由多种因素复杂相互作用的结果，包括遗传、生理、行为和环境影响。这些疾病最近的增长速度表明，环境和行为因素而非遗传因素正在推动当前的流行。在这种情况下，健康和疾病的发育起源假说强调了围孕期、胎儿期和婴儿早期与随后成年肥胖和代谢综合征发展之间的联系。尽管机制尚未完全阐明，但这种编程通常被认为是发育轨迹的不可逆变化。最近的动物模型研究表明，通过在发育可塑性期间进行营养或靶向治疗干预，代谢疾病的发育编程具有潜在的可逆转性。这篇综述将讨论发育可塑性的关键窗口期，并探讨在不良的早期环境后改善出生后代谢性疾病发展的可能途径。
