慢性压力和代谢失调对炎症性肠病的神经生物学影响。

IF 2.9 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Aleksandar Sic, Kiana Cvetkovic, Eshanika Manchanda, Nebojsa Nick Knezevic
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引用次数: 0

摘要

慢性压力是影响现代社会的一个重要因素,对身心健康有着深远的影响。皮质醇是压力反应的核心,它是一种由肾上腺分泌的糖皮质激素。虽然皮质醇的释放在急性应激反应中具有适应性,但长期暴露于高水平的皮质醇会导致不良影响。本手稿探讨了慢性应激的神经生物学意义及其对代谢失调的影响,尤其是对炎症性肠病(IBD)的影响。下丘脑-垂体-肾上腺(HPA)轴调节皮质醇的分泌,而皮质醇会影响新陈代谢、免疫反应和神经生物学。皮质醇水平升高与 IBD 等代谢性疾病的发生和恶化有关,并导致神经退行性过程,包括认知障碍和对精神疾病的易感性增加。皮质醇与其受体(尤其是糖皮质激素受体)之间的相互作用凸显了这些效应的复杂性。本综述旨在阐明慢性压力和皮质醇失调影响代谢健康和神经生物学功能的机制,为减轻这些影响的潜在治疗策略提供见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neurobiological Implications of Chronic Stress and Metabolic Dysregulation in Inflammatory Bowel Diseases.

Chronic stress is a significant factor affecting modern society, with profound implications for both physical and mental health. Central to the stress response is cortisol, a glucocorticoid hormone produced by the adrenal glands. While cortisol release is adaptive in acute stress, prolonged exposure to elevated levels can result in adverse effects. This manuscript explores the neurobiological implications of chronic stress and its impact on metabolic dysregulation, particularly in the context of inflammatory bowel diseases (IBDs). The hypothalamic-pituitary-adrenal (HPA) axis regulates cortisol production, which influences metabolism, immune response, and neurobiology. Elevated cortisol levels are associated with the development and exacerbation of metabolic disorders like IBD and contribute to neurodegenerative processes, including cognitive impairments and increased susceptibility to psychiatric conditions. The interaction between cortisol and its receptors, particularly glucocorticoid receptors, underscores the complexity of these effects. This review aims to elucidate the mechanisms through which chronic stress and cortisol dysregulation impact metabolic health and neurobiological function, providing insights into potential therapeutic strategies for mitigating these effects.

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