Developmental programming of offspring obesity, adipogenesis, and appetite.
Developmental programming of offspring obesity, adipogenesis, and appetite.
复制标题
DOI：
10.1097/grf.0b013e318299c39d
复制
发表时间：
2013-09
影响因子：
1.5
通讯作者：
Desai M
中科院分区：
文献类型：
--
作者：
Ross MG;Desai M
肥胖流行的一个新认识的主要原因是患有肥胖或妊娠糖尿病的母亲所生的婴儿、宫内生长受限的新生儿以及暴露于包括双酚A在内的环境毒素的后代的发育编程效应。导致后代肥胖的机制包括下丘脑食欲途径的编程和调节脂肪生成的脂肪形成信号。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干细胞前体的改变，这些细胞被调节以增强后代肥胖。未来预防和治疗肥胖的策略必须解决早期生活环境的编程影响。
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.