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肥胖中的代谢印记

Metabolic imprinting in obesity.

作者信息

Sullivan E L, Grove K L

出版信息

Forum Nutr. 2010;63:186-194. doi: 10.1159/000264406. Epub 2009 Nov 27.

Abstract

Increasing evidence indicates that early metabolic programming contributes to escalating obesity rates in children and adults. Metabolic imprinting is involved in the establishment of set points for physiologic and metabolic responses in adulthood. Evidence from epidemiological studies and animal models indicates that maternal health and nutritional status during gestation and lactation have long-term effects on central and peripheral systems that regulate energy balance in the developing offspring. Perinatal nutrition also impacts susceptibility to developing metabolic disorders and plays a role in programming body weight set points. The states of maternal energy status and health that are implicated in predisposing offspring to increased risk of developing obesity include maternal overnutrition, diabetes, and undernutrition. This chapter discusses the evidence from epidemiologic studies and animal models that each of these states of maternal energy status results in metabolic imprinting of obesity in offspring. Also, the potential molecular mediators of metabolic imprinting of obesity by maternal energy status including glucose, insulin, leptin, inflammatory cytokines and epigenetic mechanisms are considered.

摘要

越来越多的证据表明,早期代谢编程导致儿童和成人肥胖率不断上升。代谢印记参与了成年期生理和代谢反应设定点的建立。流行病学研究和动物模型的证据表明,妊娠和哺乳期的母亲健康和营养状况对调节发育中后代能量平衡的中枢和外周系统具有长期影响。围产期营养也会影响发生代谢紊乱的易感性,并在设定体重设定点中发挥作用。与后代患肥胖风险增加相关的母亲能量状态和健康状况包括母亲营养过剩、糖尿病和营养不良。本章讨论了来自流行病学研究和动物模型的证据,即这些母亲能量状态中的每一种都会导致后代肥胖的代谢印记。此外,还考虑了母亲能量状态导致肥胖代谢印记的潜在分子介质,包括葡萄糖、胰岛素、瘦素、炎性细胞因子和表观遗传机制。

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