The Role of Hypothalamic Microglia in the Onset of Insulin Resistance and Type 2 Diabetes: A Neuro-Immune Perspective

Int J Mol Sci. 2024 Dec 7;25(23):13169. doi: 10.3390/ijms252313169.

Abstract

Historically, microglial activation has been associated with diseases of a neurodegenerative and neuroinflammatory nature. Some, like Alzheimer's disease, Parkinson's disease, and multiple system atrophy, have been explored extensively, while others pertaining to metabolism not so much. However, emerging evidence points to hypothalamic inflammation mediated by microglia as a driver of metabolic dysregulations, particularly insulin resistance and type 2 diabetes mellitus. Here, we explore this connection further and examine pathways that underlie this relationship, including the IKKβ/NF-κβ, IRS-1/PI3K/Akt, mTOR-S6 Kinase, JAK/STAT, and PPAR-γ signaling pathways. We also investigate the role of non-coding RNAs, namely microRNAs and long non-coding RNAs, in insulin resistance related to neuroinflammation and their diagnostic and therapeutic potential. Finally, we explore therapeutics further, searching for both pharmacological and non-pharmacological interventions that can help mitigate microglial activation.

Keywords: hypothalamus; insulin resistance; microglia; microglial activation; neuroinflammation; type 2 diabetes mellitus.

Publication types

  • Review

MeSH terms

  • Animals
  • Diabetes Mellitus, Type 2* / immunology
  • Diabetes Mellitus, Type 2* / metabolism
  • Diabetes Mellitus, Type 2* / pathology
  • Humans
  • Hypothalamus* / metabolism
  • Hypothalamus* / pathology
  • Insulin Resistance*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • Microglia* / immunology
  • Microglia* / metabolism
  • Microglia* / pathology
  • Neuroinflammatory Diseases / metabolism
  • Neuroinflammatory Diseases / pathology
  • Signal Transduction

Substances

  • MicroRNAs

Grants and funding

This research received no external funding.