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

## TL;DR

This study shows that electroacupuncture helps reduce obesity by activating a specific brain circuit involving the vagus nerve and GLP-1 neurons.

## Contribution

The study identifies the vagal–GLP-1–ARC neural circuit as the mechanism through which electroacupuncture suppresses appetite and reduces obesity.

## Key findings

- Electroacupuncture activates NTSGLP−1 neurons and vagal afferent fibers, reducing food intake and obesity.
- Chemogenetic activation of NTSGLP−1 neurons mimics the appetite-suppressing effects of electroacupuncture.
- Gastric vagal deafferentation reduces the effectiveness of electroacupuncture in treating obesity.

## Abstract

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.

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.

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.

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

The online version contains supplementary material available at 10.1186/s13020-025-01274-z.