ArticleAdipocyte2025
Electroacupuncture stimulation induced M1/M2 polarization in white adipose tissues by activating the Y1 receptor in obese mice to reduce chronic inflammation.
Article in Adipocyte, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- A Gut-Protective TRPV1-Neuroepithelial Axis: Electroacupuncture Reverses Intestinal Damage in Diet-Induced Obesity.Diabetes, obesity & metabolism · 2026Article
- NPY promotes macrophage polarization and hepatic fibrogenesis via PI3K/MAPK-dependent neuroimmune mechanisms.Cellular and molecular life sciences : CMLS · 2026Article
- The Serpin Superfamily in Adipose Tissue Remodeling: Molecular Drivers of Immune-Metabolic Crosstalk and Insulin Sensitivity.Biology · 2026Review
- Article
- The role of IL-17 in orchestrating macrophage polarization via NF-κB, mTOR/HIF-1α and pyroptosis in diabetes.Scientific reports · 2026Article
- Peripheral nerve-mediated glucose lowering: Mechanisms, translational strategies, and future perspectives.World journal of diabetes · 2026Review
- Effect of BMI-stratified management based on the meridian-lymph axis theory on lower extremity lymphedema after gynecological cancer surgery: a randomized controlled trial.Frontiers in oncology · 2026Article
- Electroacupuncture pretreatment alleviates myocardial ischemia injury via brown adipose tissue and BMP3b/Smad1/5 pathway in mice.Adipocyte · 2025Article
- Machine learning-assisted network pharmacology reveals that the Chaihu-Longgu-Muli decoction modulates the inflammatory microenvironment to treat perimenopausal syndrome.Frontiers in molecular biosciences · 2025Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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