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下丘脑功能在代谢性疾病中的作用及其潜在机制。

Role of hypothalamus function in metabolic diseases and its potential mechanisms.

作者信息

Zhang Xinyu, Yang Jie, Li Yilin, Li Yulin, Li Guoqi

机构信息

Beijing Anzhen Hospital of Capital Medical University, Beijing, China.

Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, China.

出版信息

PeerJ. 2025 May 29;13:e19532. doi: 10.7717/peerj.19532. eCollection 2025.

DOI:10.7717/peerj.19532
PMID:40452923
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12126972/
Abstract

The hypothalamus, a crucial neuroendocrine regulatory center, plays a significant role in the occurrence and development of metabolic diseases. Recent advances in molecular biology and imaging technology have facilitated a better understanding of the central role of the hypothalamus in the dysregulation of regulatory mechanisms. This review examines the involvement of hypothalamic nuclei in metabolic diseases, the direct effects of glucose and fat on the hypothalamus, and the influence of the hypothalamus on metabolic diseases. Furthermore, it investigates the role of the hypothalamus in the emergence and progression of metabolic disorders, including obesity and diabetes. Finally, it outlines the current research progress in treating metabolic diseases through hypothalamus regulation. This study could provide a theoretical basis for understanding the pathophysiological mechanisms of metabolic diseases and development of new treatment strategies.

摘要

下丘脑作为一个关键的神经内分泌调节中心,在代谢性疾病的发生和发展中起着重要作用。分子生物学和成像技术的最新进展有助于更好地理解下丘脑在调节机制失调中的核心作用。本综述探讨了下丘脑核团在代谢性疾病中的参与情况、葡萄糖和脂肪对下丘脑的直接影响,以及下丘脑对代谢性疾病的影响。此外,还研究了下丘脑在代谢紊乱(包括肥胖和糖尿病)的发生和发展中的作用。最后,概述了通过下丘脑调节治疗代谢性疾病的当前研究进展。这项研究可为理解代谢性疾病的病理生理机制和开发新的治疗策略提供理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e089/12126972/f027bba16268/peerj-13-19532-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e089/12126972/676699b61208/peerj-13-19532-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e089/12126972/473f38313d3c/peerj-13-19532-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e089/12126972/d2ebd2b6e2c7/peerj-13-19532-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e089/12126972/f027bba16268/peerj-13-19532-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e089/12126972/676699b61208/peerj-13-19532-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e089/12126972/473f38313d3c/peerj-13-19532-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e089/12126972/d2ebd2b6e2c7/peerj-13-19532-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e089/12126972/f027bba16268/peerj-13-19532-g004.jpg

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Nat Commun. 2025 Mar 30;16(1):3076. doi: 10.1038/s41467-025-58356-7.
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A β-hydroxybutyrate shunt pathway generates anti-obesity ketone metabolites.一条β-羟基丁酸分流途径产生抗肥胖的酮类代谢产物。
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Remodelling of the translatome controls diet and its impact on tumorigenesis.翻译组重塑调控饮食及其对肿瘤发生的影响。
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Ketogenic diet-induced bile acids protect against obesity through reduced calorie absorption.生酮饮食诱导的胆汁酸通过减少热量吸收来预防肥胖。
Nat Metab. 2024 Jul;6(7):1397-1414. doi: 10.1038/s42255-024-01072-1. Epub 2024 Jun 27.
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Ketogenic diet administration later in life improves memory by modifying the synaptic cortical proteome via the PKA signaling pathway in aging mice.生命后期生酮饮食通过 PKA 信号通路改变突触皮质蛋白质组改善衰老小鼠的记忆。
Cell Rep Med. 2024 Jun 18;5(6):101593. doi: 10.1016/j.xcrm.2024.101593. Epub 2024 Jun 5.
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Setmelanotide for the treatment of acquired hypothalamic obesity: a phase 2, open-label, multicentre trial.用于治疗获得性下丘脑肥胖的赛美曲肽:一项 2 期、开放标签、多中心试验。
Lancet Diabetes Endocrinol. 2024 Jun;12(6):380-389. doi: 10.1016/S2213-8587(24)00087-1. Epub 2024 Apr 30.
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Microglial phagolysosome dysfunction and altered neural communication amplify phenotypic severity in Prader-Willi Syndrome with larger deletion.小胶质细胞吞噬溶酶体功能障碍和神经通讯改变放大了具有较大缺失的 Prader-Willi 综合征的表型严重程度。
Acta Neuropathol. 2024 Mar 31;147(1):64. doi: 10.1007/s00401-024-02714-0.
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Cell Metab. 2024 Feb 6;36(2):438-453.e6. doi: 10.1016/j.cmet.2024.01.003.
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