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Early life origins of metabolic disease: Developmental programming of hypothalamic pathways controlling energy homeostasis

机译:代谢性疾病的早期生命起源:控制能量稳态的下丘脑途径的发展规划

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A wealth of animal and human studies demonstrate that perinatal exposure to adverse metabolic conditions - be it maternal obesity, diabetes or under-nutrition - results in predisposition of offspring to develop obesity later in life. This mechanism is a contributing factor to the exponential rise in obesity rates. Increased weight gain in offspring exposed to maternal obesity is usually associated with hyperphagia, implicating altered central regulation of energy homeostasis as an underlying cause. Perinatal development of the hypothalamus (a brain region key to metabolic regulation) is plastic and sensitive to metabolic signals during this critical time window. Recent research in non-human primate and rodent models has demonstrated that exposure to adverse maternal environments impairs the development of hypothalamic structure and consequently function, potentially underpinning metabolic phenotypes in later life. This review summarizes our current knowledge of how adverse perinatal environments program hypothalamic development and explores the mechanisms that could mediate these effects. (C) 2015 Elsevier Inc. All rights reserved.
机译:大量的动物和人体研究表明,围产期暴露于不利的代谢条件下-无论是孕妇肥胖,糖尿病还是营养不良-都会导致后代易患肥胖症。这种机制是肥胖率指数上升的一个促成因素。暴露于母体肥胖的后代体重增加通常与食欲亢进有关,暗示能量稳态的中央调节改变是根本原因。下丘脑(代谢调节的关键区域)的围产期发育是可塑性的,并且在此关键时间窗口内对代谢信号敏感。非人类灵长类动物和啮齿动物模型的最新研究表明,暴露于不利的母亲环境会损害下丘脑结构的发育,进而损害其功能,可能在以后的生活中成为代谢表型的基础。这篇综述总结了我们目前关于不良围产期环境如何影响下丘脑发育的知识,并探讨了可能介导这些作用的机制。 (C)2015 Elsevier Inc.保留所有权利。

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