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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Diabetes. Sep 15, 2026; 17(9): 118504
Published online Sep 15, 2026. doi: 10.4239/wjd.118504
Letter to the Editor: From acupoint stimulation to immunometabolic regulation: What does electroacupuncture frequency really encode in diabetic gastroparesis?
Ke-Jia Li, Yong-Wei Yu, Yang Xia
Ke-Jia Li, Yang Xia, Department of Nephrology, The First People’s Hospital of Jiashan, Jiaxing 314100, Zhejiang Province, China
Yong-Wei Yu, Department of Intensive Care Unit, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China
Co-corresponding authors: Yong-Wei Yu and Yang Xia.
Author contributions: Li KJ wrote the manuscript, Yu YW and Xia Y designed the study and revised the manuscript, and they contributed equally to this manuscript and are co-corresponding authors. All listed authors consent to the submission.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Yong-Wei Yu, Department of Intensive Care Unit, The First Affiliated Hospital, Zhejiang University School of Medicine, No. 79 Qingchun Road, Shangcheng District, Hangzhou 310003, Zhejiang Province, China. yuyongwei@zju.edu.cn
Received: January 4, 2026
Revised: January 26, 2026
Accepted: March 6, 2026
Published online: September 15, 2026
Processing time: 239 Days and 15 Hours
Abstract

This letter builds on a recent study by Fan et al, demonstrating that electroacupuncture (EA) at the Zusanli acupoint can alleviate diabetic gastroparesis by suppressing macrophage pyroptosis via cyclic GMP-AMP synthase-stimulator of interferon genes pathway inhibition. While the authors convincingly demonstrated an immune-inflammatory mechanism underlying the therapeutic effects of EA, we argue that the most important implication of this work lies in how stimulation frequency may encode biologically distinct neuromodulatory information. In this view, EA is not merely a nonspecific peripheral intervention. We propose a hypothesis-driven, non-exclusive framework in which high-frequency EA preferentially engages afferent sensory fibers and autonomic neural circuits, thereby reshaping gastric immune tone and inflammatory thresholds in the diabetic state. Local tissue activation and vascular or perfusion-related dynamics may also operate in parallel. From this perspective, attenuation of macrophage pyroptosis and downstream cyclic GMP-AMP synthase-stimulator of interferon genes signaling can be viewed as secondary consequences of broader neuroimmune and immunometabolic reprogramming initiated by frequency-dependent neural inputs. Recognizing stimulation frequency as an informational variable rather than as a simple intensity parameter offers a rational framework for optimizing EA protocols, improving reproducibility, and extending neuromodulation-based strategies to other diabetes-associated complications characterized by immune and metabolic dysregulation.

Keywords: Electroacupuncture frequency; Neuromodulation; Diabetic gastroparesis; Neuroimmune interaction; Immunometabolic regulation

Core Tip: Electroacupuncture (EA) exerts therapeutic effects beyond local acupoint stimulation. This letter proposes that stimulation frequency encodes distinct neuromodulatory information that reshapes neuroimmune and immunometabolic regulation in diabetic gastroparesis. By reframing high-frequency EA as a frequency-encoded neuromodulatory strategy rather than a nonspecific peripheral intervention, we highlight how neural signaling may secondarily attenuate inflammatory pathways such as macrophage pyroptosis. This conceptual framework bridges traditional acupuncture with modern neuromodulation science and offers a rational basis for optimizing EA protocols in diabetes-associated gastrointestinal dysfunction. Importantly, this neuromodulatory interpretation is hypothesis-generating and intended to complement, rather than replace, other plausible mechanisms, including local tissue activation and perfusion-related effects.

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