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自主神经对能量平衡和血糖稳态的控制。

Autonomic control of energy balance and glucose homeostasis.

机构信息

Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, 34141, South Korea.

出版信息

Exp Mol Med. 2022 Apr;54(4):370-376. doi: 10.1038/s12276-021-00705-9. Epub 2022 Apr 26.

DOI:10.1038/s12276-021-00705-9
PMID:35474336
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9076646/
Abstract

Neurons in the central nervous system (CNS) communicate with peripheral organs largely via the autonomic nervous system (ANS). Through such communications, the sympathetic and parasympathetic efferent divisions of the ANS may affect thermogenesis and blood glucose levels. In contrast, peripheral organs send feedback to the CNS via hormones and autonomic afferent nerves. These humoral and neural feedbacks, as well as neural commands from higher brain centers directly or indirectly shape the metabolic function of autonomic neurons. Notably, recent developments in mouse genetics have enabled more detailed studies of ANS neurons and circuits, which have helped elucidate autonomic control of metabolism. Here, we will summarize the functional organization of the ANS and discuss recent updates on the roles of neural and humoral factors in the regulation of energy balance and glucose homeostasis by the ANS.

摘要

中枢神经系统(CNS)中的神经元主要通过自主神经系统(ANS)与外周器官进行交流。通过这些交流,ANS 的交感和副交感传出分支可能会影响产热和血糖水平。相比之下,外周器官通过激素和自主传入神经向 CNS 发送反馈。这些体液和神经反馈,以及来自大脑高级中枢的神经指令,直接或间接塑造了自主神经元的代谢功能。值得注意的是,近年来小鼠遗传学的发展使人们能够更详细地研究 ANS 神经元和回路,这有助于阐明自主神经系统对代谢的控制。在这里,我们将总结 ANS 的功能组织,并讨论神经和体液因素在调节自主神经系统的能量平衡和葡萄糖稳态方面的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/070b/9076646/8bba0377753f/12276_2021_705_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/070b/9076646/85a0a48bdf73/12276_2021_705_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/070b/9076646/8bba0377753f/12276_2021_705_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/070b/9076646/85a0a48bdf73/12276_2021_705_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/070b/9076646/8bba0377753f/12276_2021_705_Fig2_HTML.jpg

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