Electroacupuncture stimulation induced M1/M2 polarization in white adipose tissues by activating the Y1 receptor in obese mice to reduce chronic inflammation

Adipocyte. 2025 Dec;14(1):2524638. doi: 10.1080/21623945.2025.2524638. Epub 2025 Jun 30.

Abstract

Chronic inflammation in obesity can induce complications such as diabetes and cardiovascular disease. Visceral adipose tissue is the main source of inflammation, but it is difficult to regulate effectively. Here, we investigated whether ES suppressed inflammation in eWAT and reduced chronic inflammation in obese individuals. We established a high-fat diet (HFD) model with C57BL/6J mice to measure chronic inflammation in obesity. In addition, the sympathetic nerve activity (SNA) was measured with the electrophysiological technique, the immunostaining and flow cytometry were used to detect the Y1 receptors in macrophage. Finally, the key role of the M1/M2 polarization in white adipose tissues by activating the Y1 receptor was verified by Y1 receptor antagonist BIBP3226. ES reduced the contents of IL-1β, TNF-α, IL-6 and TGF-β in the plasma and the mRNA expression of il-1 and tnfα in eWAT. Also, ES suppressed SNA in eWAT which regulated NPY1R receptor. In addition, ES induced M1/M2 polarization in eWAT via the Y1 receptor. The injection of a Y1 receptor (NPY1R) antagonist BIBP3226 restrained M1/M2 polarization. Further studies revealed that ES regulated sympathetic axons in eWAT to activate the Y1 receptor. This research demonstrates ES reduce chronic inflammation e mechanism is associated with the sympathetic Y1 receptor pathway, which promotes M1/M2 polarization.

Keywords: Electroacupuncture; M1/M2 polarization; Y1 receptor; obesity; visceral adipose tissue.

MeSH terms

  • Adipose Tissue, White* / metabolism
  • Animals
  • Diet, High-Fat / adverse effects
  • Electroacupuncture* / methods
  • Inflammation* / metabolism
  • Inflammation* / therapy
  • Macrophages / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Obese
  • Obesity* / metabolism
  • Obesity* / therapy
  • Receptors, Neuropeptide Y* / metabolism
  • Sympathetic Nervous System

Substances

  • Receptors, Neuropeptide Y
  • neuropeptide Y-Y1 receptor