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应激与肥胖关联中糖皮质激素和下丘脑-垂体-肾上腺轴调节:生物学、生理学及行为学维度的全面概述

Glucocorticoids and HPA axis regulation in the stress-obesity connection: A comprehensive overview of biological, physiological and behavioural dimensions.

作者信息

Lengton Robin, Schoenmakers Myrte, Penninx Brenda W J H, Boon Mariëtte R, van Rossum Elisabeth F C

机构信息

Department of Internal Medicine, Division of Endocrinology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.

Obesity Center CGG, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.

出版信息

Clin Obes. 2025 Apr;15(2):e12725. doi: 10.1111/cob.12725. Epub 2024 Dec 2.

DOI:10.1111/cob.12725
PMID:39623561
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11907100/
Abstract

Chronic stress, characterized by increased long-term exposure to the glucocorticoid hormone cortisol, is increasingly linked to obesity development. Still, various knowledge gaps persist, including on underlying pathophysiological mechanisms. The aim of the current review is to provide the latest insights on the connection between stress and obesity. We discuss three biological stress systems-the autonomic nervous system, the hypothalamus-pituitary-adrenal (HPA) axis and the immune system-and their link with obesity, with a particular focus on the HPA axis. The role of cortisol and its regulatory variations (including glucocorticoid rhythmicity and altered sensitivity) in adipose tissue biology and obesity development is discussed. Moreover, we highlight the physiological, affective, cognitive and behavioural dimensions of the stress response offering a deeper understanding of how stress contributes to obesity development and vice versa. Finally, stress as a treatment target for obesity is discussed. We conclude that the link between stress and obesity is complex and multifaceted, influenced by physiological, affective, cognitive and behavioural stress response mechanisms, which especially when chronically present, play a key role in the development of obesity and associated cardiometabolic diseases. This necessitates integrated approaches tailored to individual needs, including lifestyle modifications, behavioural interventions, psychosocial support and possible additional pharmacological interventions.

摘要

慢性应激的特征是长期暴露于糖皮质激素皮质醇的水平增加,它与肥胖的发生越来越相关。然而,仍然存在各种知识空白,包括潜在的病理生理机制方面。本综述的目的是提供关于应激与肥胖之间联系的最新见解。我们讨论了三种生物应激系统——自主神经系统、下丘脑-垂体-肾上腺(HPA)轴和免疫系统——以及它们与肥胖的联系,特别关注HPA轴。讨论了皮质醇及其调节变化(包括糖皮质激素节律性和敏感性改变)在脂肪组织生物学和肥胖发生中的作用。此外,我们强调了应激反应的生理、情感、认知和行为维度,以便更深入地理解应激如何导致肥胖的发生,反之亦然。最后,讨论了将应激作为肥胖治疗靶点的问题。我们得出结论,应激与肥胖之间的联系是复杂且多方面的,受到生理、情感、认知和行为应激反应机制的影响,这些机制尤其是在长期存在时,在肥胖及相关心脏代谢疾病的发生中起关键作用。这就需要采取根据个体需求量身定制的综合方法,包括生活方式改变、行为干预、心理社会支持以及可能的额外药物干预。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08f8/11907100/fe9335c51e73/COB-15-e12725-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08f8/11907100/5189fdc9e6d1/COB-15-e12725-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08f8/11907100/d3065e319446/COB-15-e12725-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08f8/11907100/fe9335c51e73/COB-15-e12725-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08f8/11907100/5189fdc9e6d1/COB-15-e12725-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08f8/11907100/d3065e319446/COB-15-e12725-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08f8/11907100/fe9335c51e73/COB-15-e12725-g001.jpg

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