Scholarlink

Background <p>Electroacupuncture (EA) has demonstrated efficacy in ameliorating obesity through its marked appetite-suppressing effects. This study aims to elucidate the peripheral-central communication mechanism underlying EA's appetite inhibition mediated by the “vagal afferent fiber–nucleus tractus solitarius (NTS)–hypothalamic arcuate nucleus (ARC)” neural circuit.</p> Methods <p>High-fat diet-induced obese rats received EA or transcutaneous auricular vagus nerve stimulation (taVNS) for 8 weeks. Furthermore, we employed chemogenetic approaches to activate NTS glucagon-like peptide-1 (GLP-1) neurons (NTS<sup>GLP−1</sup>) and utilized capsaicin for gastric vagal deafferentation (GVND). Outcomes included metabolic profiles, vagal electrophysiology, expression of NTS<sup>GLP−1</sup> and hypothalamic appetite-regulating neuropeptides, and neuronal activation markers.</p> Results <p>We observed reduced expression of GLP-1 in the NTS of obese rats. Chemogenetic activation of NTS<sup>GLP−1</sup> significantly suppressed appetite, mitigated obesity, and modulated hypothalamic pro-opiomelanocortin (POMC) and neuropeptide Y (NPY). Following EA intervention in obese rats, concurrent activation of NTS<sup>GLP−1</sup> and vagal afferent fibers was observed. Similar to chemogenetic NTS<sup>GLP−1</sup> activation, EA upregulated the anorexigenic peptide POMC while downregulating the orexigenic peptide NPY in the ARC. Chemogenetic inhibition of GLP-1 neurons during EA application partially inhibited its anti-obesity and anorectic effects. Further investigations revealed that both EA and taVNS effectively reduced food intake and alleviated obesity. While both interventions activated vagal pathways and NTS<sup>GLP−1</sup>, EA induced a significantly stronger activation of vagal afferent fibers compared to taVNS. Critically, GVND prior to EA application attenuated its anti-obesity effects.</p> Conclusion <p>The therapeutic benefits of EA in appetite suppression and obesity mitigation are mediated by selective regulation of the “vagal–GLP-1–ARC” neural circuit.</p> Graphical Abstracts <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Acupuncture ameliorates diet-induced obesity via the vagal–GLP-1–ARC circuit: neural mechanism of anorexigenic action

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月8日

查看全文
  • Yanan Yang,
  • Yuwei Shao,
  • Jun Tian,
  • Yuezhu Wang,
  • Ye Zhu,
  • Siying Pan,
  • Xiali Wei,
  • Linyan Jiang,
  • Xiaoke Wang,
  • Qing Shu

摘要

Background

Electroacupuncture (EA) has demonstrated efficacy in ameliorating obesity through its marked appetite-suppressing effects. This study aims to elucidate the peripheral-central communication mechanism underlying EA's appetite inhibition mediated by the “vagal afferent fiber–nucleus tractus solitarius (NTS)–hypothalamic arcuate nucleus (ARC)” neural circuit.

Methods

High-fat diet-induced obese rats received EA or transcutaneous auricular vagus nerve stimulation (taVNS) for 8 weeks. Furthermore, we employed chemogenetic approaches to activate NTS glucagon-like peptide-1 (GLP-1) neurons (NTSGLP−1) and utilized capsaicin for gastric vagal deafferentation (GVND). Outcomes included metabolic profiles, vagal electrophysiology, expression of NTSGLP−1 and hypothalamic appetite-regulating neuropeptides, and neuronal activation markers.

Results

We observed reduced expression of GLP-1 in the NTS of obese rats. Chemogenetic activation of NTSGLP−1 significantly suppressed appetite, mitigated obesity, and modulated hypothalamic pro-opiomelanocortin (POMC) and neuropeptide Y (NPY). Following EA intervention in obese rats, concurrent activation of NTSGLP−1 and vagal afferent fibers was observed. Similar to chemogenetic NTSGLP−1 activation, EA upregulated the anorexigenic peptide POMC while downregulating the orexigenic peptide NPY in the ARC. Chemogenetic inhibition of GLP-1 neurons during EA application partially inhibited its anti-obesity and anorectic effects. Further investigations revealed that both EA and taVNS effectively reduced food intake and alleviated obesity. While both interventions activated vagal pathways and NTSGLP−1, EA induced a significantly stronger activation of vagal afferent fibers compared to taVNS. Critically, GVND prior to EA application attenuated its anti-obesity effects.

Conclusion

The therapeutic benefits of EA in appetite suppression and obesity mitigation are mediated by selective regulation of the “vagal–GLP-1–ARC” neural circuit.

Graphical Abstracts