From fasting to fat reshaping: exploring the molecular pathways of intermittent fasting-induced adipose tissue remodeling

J Pharm Pharm Sci. 2024 Jul 22:27:13062. doi: 10.3389/jpps.2024.13062. eCollection 2024.

Abstract

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.

Keywords: adipose tissue remodeling; angiogenesis; intermittent fasting; obesity; sympathetic innervation.

Publication types

  • Review

MeSH terms

  • Adipose Tissue, White / metabolism
  • Animals
  • Humans
  • Intermittent Fasting* / metabolism
  • Obesity / diet therapy
  • Obesity / metabolism
  • Signal Transduction

Grants and funding

The authors declare that financial support was received for the research, authorship, and/or publication of this article. H-KS is supported by grants from Canadian Institute of Health Research (CIHR, PJT-162083, PJT-190016), Natural Sciences and Engineering Research Council (NSERC, RGPIN-2016-06610) of Canada, Diabetes Canada (OG-3-23-5715-HS), Canada Foundation for Innovation (CFI, #40249), and Sun Life Financial New Investigator Award of Banting & Best Diabetes Centre (BBDC) of the University of Toronto. NV is supported by Novo-Nordisk Studentship from Banting and Best Diabetes Centre (BBDC) of the University of Toronto and Restracomp Master’s Scholarship from The Hospital for Sick Children. QZ is supported by Doctoral Program from Chinese Scholarship Council (CSC202008340062).