Endocrinology Unit, Centre for Cardiovascular Science, University of Edinburgh, Queen's Medical Research Institute, Edinburgh, UK.
Best Pract Res Clin Endocrinol Metab. 2012 Oct;26(5):689-700. doi: 10.1016/j.beem.2012.03.007. Epub 2012 May 22.
Epidemiological evidence suggests that exposure to an adverse environment in early life is associated with an increased risk of cardio-metabolic and behavioral disorders in adulthood, a phenomenon termed 'early life programming'. One major hypothesis for early life programming is fetal glucocorticoid overexposure. In animal studies, prenatal glucocorticoid excess as a consequence of maternal stress or through exogenous administration to the mother or fetus is associated with programming effects on cardiovascular and metabolic systems and on the brain. These effects can be transmitted to subsequent generations. Studies in humans provide some evidence that prenatal glucocorticoid exposure may exert similar programming effects on glucose/insulin homeostasis, blood pressure and neurodevelopment. The mechanisms by which glucocorticoids mediate these effects are unclear but may include a role for epigenetic modifications. This review discusses the evidence for glucocorticoid programming in animal models and in humans.
流行病学证据表明，儿童早期接触不良环境与成年后患心血管代谢和行为障碍的风险增加有关，这种现象被称为“早期生活编程”。早期生活编程的一个主要假设是胎儿糖皮质激素暴露过度。在动物研究中，由于母亲压力或通过向母亲或胎儿外源性给予导致的产前糖皮质激素过多与心血管和代谢系统以及大脑的编程效应有关。这些影响可以传递给后代。人类研究提供了一些证据，表明产前糖皮质激素暴露可能对葡萄糖/胰岛素稳态、血压和神经发育产生类似的编程效应。糖皮质激素介导这些效应的机制尚不清楚，但可能包括表观遗传修饰的作用。这篇综述讨论了动物模型和人类中糖皮质激素编程的证据。
