Translational Medicine Program, The Hospital for Sick Children, Toronto, ON, Canada.
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
J Pharm Pharm Sci. 2024 Jul 22;27:13062. doi: 10.3389/jpps.2024.13062. eCollection 2024.
Obesity, characterised by excessive fat accumulation, is a complex chronic condition that results from dysfunctional adipose tissue expansion due to prolonged calorie surplus. This leads to rapid adipocyte enlargement that exceeds the support capacity of the surrounding neurovascular network, resulting in increased hypoxia, inflammation, and insulin resistance. Intermittent fasting (IF), a dietary regimen that cycles between periods of fasting and eating, has emerged as an effective strategy to combat obesity and improve metabolic homeostasis by promoting healthy adipose tissue remodeling. However, the precise molecular and cellular mechanisms behind the metabolic improvements and remodeling of white adipose tissue (WAT) driven by IF remain elusive. This review aims to summarise and discuss the relationship between IF and adipose tissue remodeling and explore the potential mechanisms through which IF induces alterations in WAT. This includes several key structural changes, including angiogenesis and sympathetic innervation of WAT. We will also discuss the involvement of key signalling pathways, such as PI3K, SIRT, mTOR, and AMPK, which potentially play a crucial role in IF-mediated metabolic adaptations.
肥胖症的特征是脂肪过度积累，是一种复杂的慢性疾病，是由于长期热量过剩导致脂肪组织功能失调扩张引起的。这导致脂肪细胞迅速增大，超过了周围神经血管网络的支撑能力，导致缺氧、炎症和胰岛素抵抗增加。间歇性禁食（IF）是一种在禁食和进食之间循环的饮食方案，已成为一种通过促进健康的脂肪组织重塑来对抗肥胖和改善代谢平衡的有效策略。然而，IF 驱动的白色脂肪组织（WAT）代谢改善和重塑的精确分子和细胞机制仍不清楚。本综述旨在总结和讨论 IF 与脂肪组织重塑之间的关系，并探讨 IF 诱导 WAT 改变的潜在机制。这包括几个关键的结构变化，包括 WAT 的血管生成和交感神经支配。我们还将讨论关键信号通路的参与，如 PI3K、SIRT、mTOR 和 AMPK，它们可能在 IF 介导的代谢适应中发挥关键作用。
