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采用间歇性禁食作为一种非药物策略来缓解肥胖诱导的下丘脑分子通路破坏。

Using Intermittent Fasting as a Non-pharmacological Strategy to Alleviate Obesity-Induced Hypothalamic Molecular Pathway Disruption.

作者信息

Oliveira Luciana da Costa, Morais Gustavo Paroschi, Ropelle Eduardo R, de Moura Leandro P, Cintra Dennys E, Pauli José R, de Freitas Ellen C, Rorato Rodrigo, da Silva Adelino Sanchez R

机构信息

Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, University of São Paulo, São Paulo, Brazil.

Laboratory of Molecular Biology of Exercise, School of Applied Sciences, University of Campinas, São Paulo, Brazil.

出版信息

Front Nutr. 2022 Mar 30;9:858320. doi: 10.3389/fnut.2022.858320. eCollection 2022.

Abstract

Intermittent fasting (IF) is a popular intervention used to fight overweight/obesity. This condition is accompanied by hypothalamic inflammation, limiting the proper signaling of molecular pathways, with consequent dysregulation of food intake and energy homeostasis. This mini-review explored the therapeutic modulation potential of IF regarding the disruption of these molecular pathways. IF seems to modulate inflammatory pathways in the brain, which may also be correlated with the brain-microbiota axis, improving hypothalamic signaling of leptin and insulin, and inducing the autophagic pathway in hypothalamic neurons, contributing to weight loss in obesity. Evidence also suggests that when an IF protocol is performed without respecting the circadian cycle, it can lead to dysregulation in the expression of circadian cycle regulatory genes, with potential health damage. In conclusion, IF may have the potential to be an adjuvant treatment to improve the reestablishment of hypothalamic responses in obesity.

摘要

间歇性禁食(IF)是一种用于对抗超重/肥胖的流行干预措施。这种情况伴有下丘脑炎症,限制了分子途径的正常信号传导,从而导致食物摄入和能量稳态失调。本综述探讨了间歇性禁食在破坏这些分子途径方面的治疗调节潜力。间歇性禁食似乎可以调节大脑中的炎症途径,这也可能与脑-微生物群轴相关,改善下丘脑对瘦素和胰岛素的信号传导,并诱导下丘脑神经元中的自噬途径,有助于肥胖患者减重。有证据还表明,当执行间歇性禁食方案时不考虑昼夜节律周期,可能会导致昼夜节律周期调节基因表达失调,从而对健康造成潜在损害。总之,间歇性禁食可能有潜力成为一种辅助治疗方法,以改善肥胖患者下丘脑反应的重建。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a0e/9014844/8a51dc960f48/fnut-09-858320-g001.jpg

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