What does this research mean for the field?

Electroacupuncture effectively suppresses appetite and mitigates obesity via modulation of the vagal-GLP-1-ARC neural circuit. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This study aims to understand how electroacupuncture helps reduce obesity by affecting appetite regulation in the brain.

January 10, 2026Chinese Medicine0 citationsOpen Access

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

Q: What is the clinical evidence from this study?

Study design: Other. Population: Diet-induced obesity (n=48). Intervention: Electroacupuncture (EA) vs. Transcutaneous auricular vagus nerve stimulation (taVNS). Primary outcome: Suppression of appetite and reduction in body weight (null, 95% CI null, p=<0.05).

YYYanan YangJilin University YSYuwei ShaoWuhan University JTJun TianWuhan University

Key Result

Electroacupuncture effectively suppresses appetite and mitigates obesity via modulation of the vagal-GLP-1-ARC neural circuit.

Key Points

This study aims to understand how electroacupuncture helps reduce obesity by affecting appetite regulation in the brain.
Induced obesity in rats using a high-fat diet and treated with electroacupuncture or transcutaneous auricular vagus nerve stimulation for 8 weeks.
Activated NTS GLP-1 neurons using chemogenetic methods and performed gastric vagal deafferentation for analysis.
Measured metabolic profiles, electrophysiology of vagal pathways, and peptide expression related to appetite regulation.
Found reduced expression of GLP-1 in the NTS of obese rats before treatment.
Activation of NTS GLP-1 neurons led to decreased appetite and reduced obesity, affecting POMC and NPY levels.
Electroacupuncture increased anorexigenic POMC and decreased orexigenic NPY levels in response to treatment.

Structured PICO

Does electroacupuncture reduce diet-induced obesity and food intake in high-fat diet-induced obese rats?

Population

48 high-fat diet-induced obese 8-week-old male Wistar rats (baseline weight 220 ± 20 g) selected from an initial cohort of 60, and 6 normal diet control rats.

Intervention

Electroacupuncture (2-Hz, 1 mA, 10 min/session, 3 times/week) or transcutaneous auricular vagus nerve stimulation (1-mA, 2/15-Hz, 30 min/day) for 8 weeks, with or without chemogenetic modulation of NTS GLP-1 neurons or gastric vagal deafferentation using capsaicin.

Comparator

High-fat diet-induced obese rats without intervention, and normal diet control rats.

Outcome

Metabolic profiles (body mass, Lee's index, 24-h food intake), vagal electrophysiology, and expression of NTS GLP-1 and hypothalamic appetite-regulating neuropeptides (POMC, NPY) at 8 weeks.surrogate

Electroacupuncture ameliorates diet-induced obesity and suppresses appetite in rats by activating the vagal-GLP-1-ARC neural circuit.

Main Result

Effect estimate: null (95% CI null)

p-value: p=<0.05

Limitations

Limited assessment of indirect calorimetry or infrared thermography for energy metabolism characterization
Technical challenges in performing definitive monosynaptic tracing
Interactions of GLP-1 with other gut-derived signals and their broader effects on thermogenesis were not fully explored.

Abstract

Abstract 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 (NTS GLP−1 ) and utilized capsaicin for gastric vagal deafferentation (GVND). Outcomes included metabolic profiles, vagal electrophysiology, expression of NTS GLP−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 NTS GLP−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 NTS GLP−1 and vagal afferent fibers was observed. Similar to chemogenetic NTS GLP−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 NTS GLP−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

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