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子代肥胖、脂肪生成和食欲的发育编程。

Developmental programming of offspring obesity, adipogenesis, and appetite.

作者信息

Ross Michael G, Desai Mina

机构信息

Perinatal Research Laboratories, Department of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, USA.

出版信息

Clin Obstet Gynecol. 2013 Sep;56(3):529-36. doi: 10.1097/GRF.0b013e318299c39d.

Abstract

A newly recognized primary cause of the obesity epidemic is the developmental programming effects of infants born to mothers with obesity or gestational diabetes, intrauterine growth-restricted newborns, and offspring exposed to environmental toxins including bisphenol A. The mechanisms which result in offspring obesity include the programming of the hypothalamic appetite pathway and adipogenic signals regulating lipogenesis. Processes include nutrient sensors, epigenetic modifications, and alterations in stem cell precursors of both appetite/satiety neurons and adipocytes which are modulated to potentiate offspring obesity. Future strategies for the prevention and therapy of obesity must address programming effects of the early life environment.

摘要

肥胖流行新发现的一个主要原因是,母亲患有肥胖症或妊娠糖尿病的婴儿、宫内生长受限的新生儿以及接触包括双酚A在内的环境毒素的后代所产生的发育编程效应。导致后代肥胖的机制包括下丘脑食欲通路的编程以及调节脂肪生成的脂肪生成信号。这些过程包括营养传感器、表观遗传修饰,以及食欲/饱腹感神经元和脂肪细胞的干细胞前体的改变,这些改变被调节以增强后代肥胖。肥胖预防和治疗的未来策略必须应对早期生活环境的编程效应。

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