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新生儿胰岛素作用会损害下丘脑神经回路的形成,这是对母亲高脂肪养的反应

Merly C Vogt¹, Lars Paeger², Simon Hess²

¹Max Planck Institute for Neurological Research, 50931 Cologne, Germany; Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.

|January 28, 2014

概括

哺乳期母亲的高脂肪饮食通过破坏下丘脑神经投影,为肥胖的后代制定了计划. 恢复后代神经元中的胰岛素信号,可以防止这些代谢中断.

科学领域:

神经科学是一个神经科学.
代谢研究研究代谢研究
发展生物学发展生物学

背景情况:

母亲的代谢健康显著影响后代的长期健康.
在关键发育窗口期间高脂肪饮食 (HFD) 可能导致代谢功能障碍.

研究的目的:

为了研究母乳养期间母乳高血压如何影响后代的新陈代谢平衡和下丘脑电路.
确定胰岛素信号传递在调解这些效应中的作用.

主要方法:

在哺乳期,小鼠被食HFD.
评估后代的肥胖和葡萄糖平衡.
分析了下丘脑的黑色素皮质蛋白电路,包括proopiomelanocortin (POMC) 和agouti相关 (AgRP) 神经元及其投影.
利用基因操纵在POMC神经元中取消胰岛素作用.

主要成果:

哺乳期母亲的HFD导致后代肥胖和葡萄糖平衡受损.
脑下垂体POMC和AgRP神经元的功能和表达不受影响,但它们的预测受损.
在后代POMC神经元中取消胰岛素作用可以防止改变预测和代谢缺陷.

结论:

哺乳期母亲的HFD通过损害下丘脑神经元投射来破坏后代的新陈代谢平衡.
后代POMC神经元中的胰岛素信号传递对于预防由母亲过度营养引起的代谢功能障碍至关重要.

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