Metabolic imprinting in obesity.

Forum of Nutrition Pub Date : 2010-01-01 Epub Date: 2009-11-27 DOI:10.1159/000264406
E L Sullivan, K L Grove
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引用次数: 126

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.

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肥胖的代谢印记。
越来越多的证据表明,早期代谢程序导致儿童和成人肥胖率不断上升。代谢印记涉及成年期生理和代谢反应设定值的建立。来自流行病学研究和动物模型的证据表明,孕期和哺乳期的孕产妇健康和营养状况对调节发育中的后代能量平衡的中枢和外周系统具有长期影响。围产期营养还会影响代谢紊乱的易感性,并在设定体重设定值方面发挥作用。母亲的能量状态和健康状态包括营养过剩、糖尿病和营养不良,与后代肥胖风险增加有关。本章讨论了来自流行病学研究和动物模型的证据,这些证据表明,母亲能量状态的每一种状态都会导致后代肥胖的代谢印记。此外,还考虑了母体能量状态下肥胖代谢印迹的潜在分子介质,包括葡萄糖、胰岛素、瘦素、炎症细胞因子和表观遗传机制。
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Metabolic imprinting in obesity. Do leptin and insulin signal adiposity? Leptin-signaling pathways and leptin resistance. Hypothalamic-brainstem circuits controlling eating. Brainstem integrative function in the central nervous system control of food intake.
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