Endocrinology Unit, Centre for Cardiovascular Science, University of Edinburgh, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, United Kingdom.
J Steroid Biochem Mol Biol. 2010 Oct;122(1-3):3-9. doi: 10.1016/j.jsbmb.2010.01.009. Epub 2010 Feb 1.
Epidemiological studies have shown that low birthweight is associated with increased risk of development of diabetes and obesity in later life. Over-exposure of the developing fetus to glucocorticoids is one of the major hypotheses that has been proposed to explain this association. In animal models, a range of manipulations that increase fetal glucocorticoid load, 'programme' permanent changes in glucose and insulin metabolism and adiposity. This may be mediated by alterations in regulation of the hypothalamic-pituitary-adrenal (HPA) axis. In humans, low birthweight is associated with increased circulating glucocorticoid levels, and an increased cortisol response to physiological and psychosocial stressors, in child- and adulthood. This activation of the HPA axis is also associated with increased risk of development of diabetes and obesity in later life.
流行病学研究表明，低出生体重与日后发生糖尿病和肥胖的风险增加有关。过度暴露于发育中的胎儿糖皮质激素是解释这种关联的主要假说之一。在动物模型中，一系列增加胎儿糖皮质激素负荷的操作“编程”了葡萄糖和胰岛素代谢及肥胖的永久性改变。这种改变可能是通过调节下丘脑-垂体-肾上腺（HPA）轴来介导的。在人类中，低出生体重与儿童期和成年期循环中糖皮质激素水平升高以及对生理和心理应激源的皮质醇反应增强有关。HPA 轴的这种激活也与日后发生糖尿病和肥胖的风险增加有关。
