Background Obesity is closely associated with chronic low-grade inflammation, particularly within visceral adipose tissues (VAT). Dendritic cells (DCs), as key antigen-presenting cells, bridge innate and adaptive immunity and play a pivotal role in regulating adipose tissue immune homeostasis. This study aims to investigate the effects and underlying mechanisms of electroacupuncture (EA) on obesity-associated inflammation, with a particular focus on DCs migration. Methods A high-fat diet (HFD) was used to induce obesity in C57BL/6 mice. Electroacupuncture (EA) was administered to obese mice, and body weight and adipose tissue morphology were assessed. Hematoxylin and eosin (H&E) staining, Western blotting (WB), enzyme-linked immunosorbent assay (ELISA), immunofluorescence (IF), and flow cytometry were employed to evaluate the inflammatory status and immune cell infiltration in mesenteric adipose tissue (MAT). CM-DiI tracing and CCR7 pathway analyses were conducted to investigate DCs migration. Results EA significantly reduced body weight and alleviated adipose tissue inflammation in obese mice. H&E staining revealed improved adipocyte morphology in MAT following EA treatment. ELISA and WB showed decreased levels of pro-inflammatory cytokines (TNF-α, IL-1β) in serum and MAT. IF analysis indicated reduced macrophage and T-cell infiltration in EA-treated groups. Flow cytometry demonstrated decreased DCs accumulation in mesenteric lymph nodes(MLNs) and MAT. CM-DiI tracing confirmed that EA suppressed intestinal DCs migration into MAT. Furthermore, EA downregulated CCR7 expression in intestinal tissue, suggesting an association between EA treatment and altered CCR7-associated DCs trafficking. Conclusion Acupuncture ameliorates obesity-induced inflammatory responses by reducing the migration of intestinal DCs to MAT, potentially through modulation of CCR7-associated signaling pathways. These findings provide novel insights into the immunomodulatory mechanisms of acupuncture and support its therapeutic potential in metabolic inflammation.

The Dawn Phenomenon (DP) denotes the occurrence of spontaneous early-morning hyperglycemia in the absence of overnight hypoglycemia, or that necessitating an elevation in insulin to sustain normal morning blood glucose levels. Studies exhibit considerable variability, with some indicating that DP is a spontaneous occurrence reported in a substantial percentage of individuals. Patients with DP demonstrate increased average blood glucose variability over a 24-h period compared to those without DP, presenting considerable problems for clinical diabetes pharmacotherapy and nutritional regulation. Moreover, given the ambiguity surrounding the precise pathophysiology and targeted therapies for DP, therapeutic care predominantly emphasizes symptom alleviation. Conventional perspectives ascribe DP to physiological surges in the secretion of counterregulatory hormones, including cortisol, catecholamines, and growth hormone, in the early morning hours. These hormones enhance hepatic glucose production while concurrently diminishing peripheral tissue sensitivity to insulin. This article examines the contemporary pathophysiological underpinnings of DP to offer insights for clinical diagnosis and treatment in diabetes. This article focuses mainly on the dawn phenomenon in type 2 diabetes (T2DM), while evidence related to type 1 diabetes (T1DM) is addressed independently.

Objective: To report the long-term follow-up outcomes of Jiao’s scalp acupuncture in a patient with cervical spinal cord injury, with emphasis on spasticity control and sustained functional recovery following an initial phase of improvement. Methods: This case represents a continuation of a previously reported patient with traumatic cervical spinal cord injury who underwent integrative acupuncture therapy. In the present follow-up phase, the treatment strategy was refined to emphasize scalp acupuncture targeting the Motor Area and Tremor Control Area, combined with auricular and body acupuncture. Treatments were administered once weekly over a six-month period. Results: During this follow-up phase, progressive neurological and functional improvements were observed. Involuntary limb spasms decreased after 2–3 sessions. By sessions 6–8, the patient regained ambulation without assistive devices, and by session 12, independent walking under supervision was achieved. Within two months, improvements in muscle tone, joint range of motion, and functional mobility were noted. Muscle strength improved from 1/5 to 4/5 on the Medical Research Council (MRC) scale. Conclusion: This follow-up report suggests that Jiao’s scalp acupuncture may contribute not only to initial neurological recovery but also to long-term maintenance and modulation of motor function in patients with chronic cervical spinal cord injury. Further studies are warranted to investigate its role in sustained neurorehabilitation.

PurposeSemaglutide is effective for type 2 diabetes mellitus (T2DM) but limited by dose-dependent gastrointestinal adverse effects. As electroacupuncture (EA) possesses glucose-lowering effects, this study investigates the therapeutic potential and mechanism of combining EA with semaglutide to facilitate dose reduction while maintaining efficacy.MethodsMale db/db mice were divided into: the model group(T2DM), the high/normal/low-dose semaglutide group (SH, SN, SL), the normal/low-dose semaglutide + EA at ST25 group (ST25N, ST25L), and the EA at ST25 group (ST25). The db/m mice served as the control group (CON). Blood glucose regulation was assessed via random/fasting blood glucose and oral glucose tolerance test (OGTT). To evaluate glycemic control and lipid profiles, HbA1c and insulin levels were quantified via ELISA, and T-CHO, TG, LDL-C, and HDL-C via biochemical kits. GLP-1R expression and β-cell abundance were assessed by immunofluorescence, and pancreatic apoptosis by TUNEL staining. PKA, pPKA, Bcl-2, Bax, and GLP-1R were analyzed by Western blot. Male Sprague–Dawley (SD) rats were separated into 2 groups: the normal-dose semaglutide rats group (RSN) and the normal-dose semaglutide + EA at ST25 rats group (RST25N). LC-MS/MS was employed to measure the concentrations of semaglutide in the plasma and pancreas, thereby evaluating the influence of EA.ResultsEA enhances the effects of semaglutide on improving glycemic control and lipid metabolism, with significant reductions in random/fasting blood glucose, HbA1c, TCHO, TG and LDL-C levels, improvements in OGTT, insulin and HDL-C levels, and longer duration of controlled blood glucose within the target range, Furthermore, EA combined with semaglutide showed a marked increase in pancreatic β-cells, with the increased expression of pancreatic GLP-1R, PKA, pPKA and Bcl-2, the reduced expression of Bax, increased concentration of semaglutide in plasma and pancreas.ConclusionEA combined with normal- or low-dose semaglutide achieved glycemic control comparable to, or even better than, high-dose semaglutide alone, and its mechanism may be related to its enhancement of GLP-1R to inhibit β-cell apoptosis and the increased concentration of semaglutide in plasma and pancreas. EA thus has great potential to reduce the dose of semaglutide to alleviate its side effects while ensuring its clinical efficacy.

ObjectiveTo observe the correlation between referred hyperaesthesia and acupoint sensitization in kidney diseases patients and to investigate the rule of regional sensitized point distribution in rats.MethodsA total of 158 kidney-related diseases patients from 5 hospitals in China were recruited in the present study. The tenderness was palpated along the chest， back， shoulder， upper limbs， lower limbs，etc. by specially-assigned researcher in each hospital. In animal experiments， experimental group rats（n=8） received an injection of 10% mustard oil into subcortical region of the right kidney to trigger renal inflammation， while the control group rats（n=9） received an injection of saline solution into subcortical region of the right kidney. All the rats accepted tail venous injection of 5% Evans blue for examining the distribution of the blue dye exudation spots at the body surface.ResultsThe tenderness spots were found at the abdomen， waist， buttock， lower limbs and primarily concentrated in the T9—L4 and S2 spinal segments. The location of referred pain overlaps with acupoints. In experimental rats， cutaneous exudation points were distributed across the abdomen， lumbar-dorsal region， and sacral area， corresponding to the dermatomal regions innervated by the T7—L5 spinal segments.ConclusionIn the case of kidney diseases， a regular “referred sensitization” response frequently occurs in the dermatomere area innervated by the corresponding T8—L1 segments and adjacent nerve distribution areas.

Glucose homeostasis is crucial for metabolic health, with disruptions leading to hyperglycemia (e.g., diabetes affecting over 589 million adults worldwide in 2025) or hypoglycemia, both associated with severe complications like nephropathy, neuropathy, and cardiovascular disease. The peripheral nervous system (PNS) is a less studied regulator of glucose balance through neural circuits involving the sympathetic, parasympathetic, sensory, and somatic nerves, which interact with organs like the liver, pancreas, and gut. This review aims to synthesize recent advances in PNS-mediated glucose lowering, covering mechanistic foundations, organ-specific pathways, translational interventions (e.g., device-based neuromodulation, pharmacological approaches, closed-loop systems, and regenerative strategies), preclinical/clinical evidence, translational challenges, and future perspectives to provide a roadmap for developing novel, drug-free therapies for dysglycemia.

BACKGROUND Diabetic peripheral neuropathy (DPN) is a common chronic complication of diabetes, and current therapeutic options remain unsatisfactory. Mitochondrial dysfunction is considered a key contributor to DPN, and modulation of mitochondrial biogenesis may represent a promising therapeutic strategy. Electroacupuncture (EA) has shown beneficial effects in diabetic neuropathy, but its underlying mechanisms remain incompletely understood. We hypothesized that EA alleviates type 2 DPN (T2DPN) by enhancing silent information regulator 1 (SIRT1)/peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α)-mediated mitochondrial biogenesis and mitochondrial redistribution, particularly in intraepidermal nerve fibers (IENFs). AIM To investigate whether EA alleviates T2DPN through SIRT1/PGC-1α-mediated mitochondrial biogenesis and redistribution. METHODS A rat model of T2DPN was established by high-fat diet feeding combined with streptozotocin injection (35 mg/kg). After successful model establishment, rats received EA stimulation at ST25 for 6 weeks. Metabolic parameters, behavioral tests, nerve conduction studies, immunofluorescence staining, western blotting, and three-dimensional imaging were used to evaluate mitochondrial content and distribution in IENFs and sciatic nerve tissue, as well as SIRT1 and PGC-1α expression. RESULTS Changes in body weight, blood glucose, behavioral responses, and nerve conduction confirmed the successful establishment of the T2DPN model. EA improved metabolic status, increased withdrawal thresholds, and ameliorated IENF loss, indicating protective effects on neural function and morphology. In T2DPN rats, SIRT1/PGC-1α-mediated mitochondrial biogenesis was reduced. EA treatment upregulated SIRT1 and PGC-1α expression in the sciatic nerve and increased mitochondrial content. Three-dimensional analysis showed more prominent mitochondrial redistribution in IENFs than in adjacent keratinocytes. In addition, SIRT1 inhibition attenuated the beneficial effects of EA on nerve function, while showing limited effects on systemic metabolic parameters. CONCLUSION EA protects against T2DPN and is associated with SIRT1/PGC-1α-mediated mitochondrial biogenesis and redistribution, with neural benefits partly dissociated from metabolic regulation.

BACKGROUND:Organ transplantation has emerged as a globally prevalent therapeutic modality for end-stage organ failure, yet the post-transplantation trajectory is increasingly complicated by a spectrum of metabolic sequelae, with obesity emerging as a critical clinical challenge. AIM:To systematically review the multifactorial mechanisms underlying obesity following organ transplantation and to integrate evidence from pharmacological, behavioral, and molecular perspectives, thereby providing a foundation for targeted interventions. METHODS:We conducted a systematic search in PubMed and Web of Science for literature published from 2020 to 15 July 2025. The search strategy incorporated terms including "obesity", "overweight" and "post organ transplantation". Only randomized controlled trials, meta-analyses, and systematic reviews were included. Non-empirical publications and irrelevant studies were excluded. Data extraction and quality assessment were performed by two independent reviewers, with disagreements resolved by a third researcher. RESULTS:A total of 1457 articles were initially identified, of which 146 met the inclusion criteria. These studies encompassed liver, kidney, heart, and lung transplant recipients. Key findings indicate that immunosuppressive drugs-especially corticosteroids and calcineurin inhibitors-promote hyperphagia, insulin resistance, and dyslipidemia. Post-transplant sedentary behavior and hypercaloric diets further contribute to positive energy balance. At the molecular level, immunosuppressants disrupt adipokine signaling (e.g., leptin and adiponectin), induce inflammatory and oxidative stress responses, and activate adipogenic pathways leading to lipid accumulation. CONCLUSION:Post-transplant obesity arises from a complex interplay of pharmacological, behavioral, and molecular factors. A multidisciplinary approach-incorporating pharmacological modification, nutritional management, physical activity, and molecular-targeted therapies-is essential to mitigate obesity and improve transplant outcomes. Further large-scale and mechanistic studies are warranted to establish evidence-based preventive and treatment strategies.

This article synthesizes current evidence to elucidate the role of pancreatic macrophage metabolic memory in linking obesity to type 2 diabetes. Through an integrated analysis of recent studies, we describe how metabolic stress reprograms pancreatic macrophages toward a spectrum of inflammatory phenotypes and establishes persistent memory via epigenetic and exosomal pathways. This memory sustains pro-inflammatory signaling even after metabolic insults cease, leading to impaired β-cell function and dedifferentiation through altered transcriptional regulation and paracrine communication. We conclude that targeting this macrophage memory axis offers a promising therapeutic strategy, with interventions such as exercise, natural products, and epigenetic modulators showing potential to reverse maladaptive polarization. Future research using single-cell omics will be essential to decode macrophage heterogeneity and advance memory-targeted therapies. During the transition from obesity to type 2 diabetes, the islets are often accompanied by persistent inflammation. The metabolic memory formed by pancreatic macrophages may be the core cell-intrinsic mechanism underlying the long-term maintenance of this phenomenon. That is, macrophages, through epigenetic reprogramming, “remember” prior metabolic stress. Even after the external stimuli subside, their pro-inflammatory phenotype continues to be sustained, thereby driving the macroscopically observed state of persistent inflammation. These two phenomena constitute a causal relationship. This concept is distinct from classical “trained immunity”, which refers to the enhanced response of immune cells to a heterologous secondary stimulus, focusing on the boosting of defensive functions. This study primarily utilized the PubMed database for retrieval, employing keywords such as “pancreas”, “metabolic memory” and “macrophage” for subject term searches. It screened for mechanism-based articles and review papers concerning metabolic memory in pancreatic macrophages.

Aim Obesity impairs the colonic mucus layer and disrupts intestinal barrier function, leading to chronic inflammation. This study explores whether electroacupuncture can restore intestinal barrier integrity and alleviate chronic intestinal inflammation by promoting goblet cell mucus secretion via the TRPV1-CGRP-RAMP1 axis. It also examines the underlying mechanisms of sensory neuron. Epithelial cell crosstalk in this process, with the goal of providing a new interventional strategy for treating obesity-related intestinal barrier damage and metabolic inflammation.Materials and Methods In a high-fat diet (HFD)-induced obesity model using C57BL/6J mice, we employed tissue-clearing techniques to examine the expression of TRPV1 and CGRP in intact colon tissue. The expression of RAMP1 in goblet cells was assessed by immunohistochemistry. Colon pathology was evaluated using immunofluorescence, haematoxylin and eosin (H&E) staining, and Alcian blue-periodic acid-Schiff (AB-PAS) staining. Furthermore, western blot analysis was performed to measure the expression levels of tight junction proteins and proinflammatory cytokines in the colon tissue.Results HFD feeding resulted in increased intestinal permeability and aggravation of intestinal inflammation. Notably, electroacupuncture intervention reversed HFD-induced intestinal pathologies. Through targeted ablation of TRPV1 and administration of the RAMP1 antagonist BIBN4096, we further established the essential roles of TRPV1 signalling and the CGRP receptor RAMP1 in maintaining mucus layer thickness and intestinal homeostasis. Under these conditions, the therapeutic efficacy of electroacupuncture was abolished.Conclusions We demonstrated that electroacupuncture may promote mucus secretion from goblet cells via the TRPV1-CGRP-RAMP1 axis, thereby suppressing intestinal inflammation. This provides a feasible interventional strategy for treating obesity-related intestinal barrier damage.

OBJECTIVES:To investigate the mechanism by which electroacupuncture (EA) at "Zusanli" (ST36) ameliorates the impairment of feeding behavior and gastric vagal afferent signaling induced by short-term high-fat diet (HFD) exposure. METHODS:The study comprised two parts. In part 1, 42 SPF male C57BL/6J mice were randomly divided into a normal diet (ND) group (n=14) and an HFD group (n=28). After 4 weeks, HFD-fed mice were subdivided into an HFD group and an EA group (n=14 each). The EA group received EA at bilateral "Zusanli" (ST36). Stimulation parameters were:2 mA, 2 Hz/15 Hz, 20 min/session, once daily, 6 sessions/week for 2 consecutive weeks. Body weight was recorded weekly. After the intervention, 24 h food intake was measured. Liver wet weight, inguinal white adipose tissue (iWAT) wet weight, and epididymal white adipose tissue (eWAT) wet weight were recorded. Gastric emptying rate was assessed using the phenol red meal test. Serum cholecystokinin (CCK) content was measured by ELISA. Protein expressions of protein gene product 9.5 (PGP9.5) and calcitonin gene-related peptide (CGRP) in the gastric antrum were evaluated by Western blot. The co-expression density index of PGP9.5 and CGRP in the gastric antrum and c-Fos expression levels in the nodose ganglion (NG) were detected by immunofluorescence staining. In part 2, another 32 SPF male C57BL/6J mice were fed an HFD for 4 weeks and then randomly divided into 4 groups (n=8 each):sham operation group, sham + EA group, vagotomy (resection of the gastric vagal branches) group, and vagotomy + EA group. The acupoint and intervention parameters were the same as above. Body weight, 24 h food intake, liver wet weight, iWAT wet weight, eWAT wet weight, the co-expression of PGP9.5 and CGRP in the gastric antrum, and the number of c-Fos positive neurons in the NG were measured. RESULTS:Compared to the ND group, 4-week HFD feeding increased body weight, liver wet weight, and adipose tissue (iWAT and eWAT) wet weights, while decreased gastric emptying rate and serum CCK levels(P<0.05). The relative protein expressions of both PGP9.5 and CGRP in the gastric antrum were down-regulated(P<0.05). Meanwhile, the co-expression density index of PGP9.5 and CGRP in the gastric antrum was reduced(P<0.05). The number of c-Fos positive neurons in the NG decreased in HFD-fed mice(P<0.05). Compared to the HFD group, EA treatment reduced body weight, 24 h food intake, liver wet weight, and adipose tissue (iWAT and eWAT) wet weights(P<0.05). EA also increased gastric emptying rate and serum CCK levels(P<0.05). Moreover, EA up-regulated the relative protein expressions of PGP9.5 and CGRP as well as their co-expression density index in the gastric antrum(P<0.05). Finally, EA increased the number of c-Fos positive neurons in the NG(P<0.05). In the vagotomy experiment, compared with the sham operation group, the sham{L-End} +{L-End} EA group showed a significant decrease in body weight, food intake, liver wet weight, adipose tissue wet weight (P<0.05). After gastric branch vagotomy, however, the regulatory effects of EA on body weight, food intake, liver wet weight, and other indicators were weakened. Similarly, after surgery EA did not exert a significant modulatory effect on the co-expression level of PGP9.5 and CGRP in the gastric antrum or on the expression of c-Fos-positive neurons in the NG. CONCLUSIONS:Short-term HFD leads to desensitization of gastric vagal afferent signaling, manifested as impairment of local gastric vagal sensory nerves and a decrease in the number of activated neurons in the NG. EA can suppress food intake by repairing gastric vagal afferent signaling.

BACKGROUND:Metformin (Met) is a first-line pharmacological treatment for type 2 diabetes mellitus (T2DM). The potential effect of combining electroacupuncture (EA) at ST25 (Tianshu) with Met in ameliorating intestinal injury remains largely unexplored. METHODS:We established wild-type (Control) and diabetic model groups that remained untreated (Model), received EA only (EA), received Met treatment only (Met) or received EA combined with Met (EA + Met), and compared markers of intestinal injury and insulin resistance, as well as effects on signal transducer and activator of transcription (STAT) proteins and microRNAs. RESULTS:EA and Met treatment (alone and in combination) had positive effects on fasting plasma glucose, fasting insulin levels, Homeostatic Model Assessment-insulin resistance (HOMA-IR) indices and stool number, while fecal water content was positively impacted by EA treatment (with or without concurrent Met) but not Met alone. Hematoxylin-eosin staining demonstrated that both EA alone and EA in combination with Met appeared to repair intestinal damage in the jejunum, ileum and colon. In addition, enzyme-linked immunosorbent assay revealed that serum interleukin 10 levels were restored in all treatment groups. Furthermore, quantitative real-time polymerase chain reaction (PCR) analysis revealed that EA at ST25 resulted in the activation of STAT5A in the jejunum, as well as STAT5A, STAT5B and STAT6 in the ileum. Notably, in the EA + Met group, there was a specific enhancement of STAT2, STAT3 and STAT5B in the colon, indicating segment-specific activation within distinct regions of the intestine. CONCLUSION:EA at ST25 may ameliorate intestinal injury via the Janus kinase (Jak)/STAT signaling pathway and is closely related to jejunal and ileal segments. These findings provide a theoretical basis for EA combined with medication.

Due to its benefits of minimum physiological interference, few complications, and promotion of postoperative recovery, acupuncture-assisted anesthesia (AA), an inventive fusion of modern anesthesiology and traditional Chinese medicine, has been used more frequently in clinical surgical practice. This review systematically summarizes the specific operational techniques and technical details of AA across various surgical procedures. Mechanistically, AA produces analgesia, sedation, and organ protection through modulation of the nervous, endocrine, and immune systems. In terms of operational specifications, auricular points are primarily stimulated via acupressure or needling at Shenmen (TF4) and surgical site-specific reflex zones, while body acupoints including Hegu (LI4), Zusanli (ST36), and Neiguan (PC6) are selected according to local, distant, and empirical principles, combined with standardized electroacupuncture parameters (frequency, intensity, and waveform). Clinical evidence demonstrates that auricular acupuncture reduces intraoperative fentanyl requirement by 15% compared with sham acupuncture. These clinical benefits depend on the standardized implementation of the following practices: Preoperative formulation of individualized acupoint combinations based on surgical type and patient constitution, intraoperative application of 2/100 Hz dense-disperse electroacupuncture at appropriate intensity, and postoperative continuation of auricular acupressure to consolidate analgesic effects and promote gastrointestinal recovery. To give clinicians a standardized, useful reference to enhance the safety and efficacy of AA application and encourage the thorough integration of traditional Chinese medicine and contemporary surgical anesthesia, the present difficulties and future development directions of AA in surgical practice are finally outlined.

Objective To observe the role of leptin receptor (LepR) in the dorsal vagal complex (DVC) in electroacupuncture (EA)-mediated regulation of food intake, so as to explore its central mechanism underlying improvement of metabolic disorders. Methods Ten C57BLKS/JGpt mice were randomly selected as the normal group, and the remaining mice were fed with high-fat diet (HFD) to establish a obesity model. Successfully modeled mice were randomly divided into the HFD group and EA group, with 10 mice in each group. The EA group received EA stimulation (2 mA, 2 Hz/15 Hz) at bilateral u201CZusanliu201D (ST36) for 20 min, once daily, 6 times per week, for 5 weeks. The body weight, food intake, liver tissue wet weight, inguinal white adipose tissue (iWAT) weight, epididymal white adipose tissue (eWAT) and brown adipose tissue (BAT) weight, and blood glucose levels were measured. The serum insulin and leptin contents were measured using ELISA. Immunofluorescence staining was used to detect the co-expression of LepR and proto-oncogene c-Fos protein (c-Fos), the expression of phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in the nucleus tractus solitarii (NTS) and dorsal motor nucleus of the vagus nerve (DMV), and the co-expression of choline acetyltransferase (ChAT) and c-Fos in DMV. Results Compared with the normal group, the HFD group showed a significant increase in the body weight, liver and adipose (iWAT, eWAT and BAT) wet weight, serum insulin and leptin contents, fasting blood glucose level, and glucose tolerance area under the curve (AUC, Pu0026lt;0.01), the number of LepR and c-Fos co-expression neurons in the DMV and NTS, p-STAT3 positive and ChAT and c-Fos co-expression neurons in the DMV were remarkably decreased (Pu0026lt;0.05, Pu0026lt;0.01). In comparison with the HFD group, the body weight, food intake, liver and adipose wet weight, serum leptin content, fasting blood glucose, and glucose tolerance AUC were significantly decreased in the EA group (Pu0026lt;0.01), while the number of LepR and c-Fos co-expression neurons in the DMV and NTS, p-STAT3 positive and ChAT and c-Fos co-expression neurons in the DMV were notably increased in the EA group (Pu0026lt;0.05, Pu0026lt;0.01). No significant differences were observed in the random blood glucose content and p-STAT3 positive expression in the NTS among the three groups and in the serum level of insulin after EA. Conclusion EA at ST36 can inhibit food intake and reduce body weight in obesity mice, which may be associated with restoration of LepR-ralated signaling in the DVC and improvement of cholinergic vagal efferent neuronal activity in the DMV.

Objective To investigate the mechanism by which electroacupuncture (EA) at u201CZusanliu201D (ST36) ameliorates the impairment of feeding behavior and gastric vagal afferent signaling induced by short-term high-fat diet (HFD) exposure. Methods The study comprised two parts. In part 1, 42 SPF male C57BL/6J mice were randomly divided into a normal diet (ND) group (n=14) and an HFD group (n=28). After 4 weeks, HFD-fed mice were subdivided into an HFD group and an EA group (n=14 each). The EA group received EA at bilateral u201CZusanliu201D (ST36). Stimulation parameters were: 2 mA, 2 Hz/15 Hz, 20 min/session, once daily, 6 sessions/week for 2 consecutive weeks. Body weight was recorded weekly. After the intervention, 24 h food intake was measured. Liver wet weight, inguinal white adipose tissue (iWAT) wet weight, and epididymal white adipose tissue (eWAT) wet weight were recorded. Gastric emptying rate was assessed using the phenol red meal test. Serum cholecystokinin (CCK) content was measured by ELISA. Protein expressions of protein gene product 9.5(PGP9.5) and calcitonin gene-related peptide (CGRP) in the gastric antrum were evaluated by Western blot. The co-expression density index of PGP9.5 and CGRP in the gastric antrum and c-Fos expression levels in the nodose ganglion (NG) were detected by immunofluorescence staining. In part 2, another 32 SPF male C57BL/6J mice were fed an HFD for 4 weeks and then randomly divided into 4 groups (n=8 each): sham operation group, sham + EA group, vagotomy (resection of the gastric vagal branches) group, and vagotomy + EA group. The acupoint and intervention parameters were the same as above. Body weight, 24 h food intake, liver wet weight, iWAT wet weight, eWAT wet weight, the co-expression of PGP9.5 and CGRP in the gastric antrum, and the number of c-Fos positive neurons in the NG were measured. Results Compared to the ND group, 4-week HFD feeding increased body weight, liver wet weight, and adipose tissue (iWAT and eWAT) wet weights, while decreased gastric emptying rate and serum CCK levels (Pu0026lt;0.05). The relative protein expressions of both PGP9.5 and CGRP in the gastric antrum were down-regulated (Pu0026lt;0.05). Meanwhile, the co-expression density index of PGP9.5 and CGRP in the gastric antrum was reduced (Pu0026lt;0.05). The number of c-Fos positive neurons in the NG decreased in HFD-fed mice (Pu0026lt;0.05). Compared to the HFD group, EA treatment reduced body weight, 24 h food intake, liver wet weight, and adipose tissue (iWAT and eWAT) wet weights (Pu0026lt;0.05). EA also increased gastric emptying rate and serum CCK levels (Pu0026lt;0.05). Moreover, EA up-regulated the relative protein expressions of PGP9.5 and CGRP as well as their co-expression density index in the gastric antrum (Pu0026lt;0.05). Finally, EA increased the number of c-Fos positive neurons in the NG (Pu0026lt;0.05). In the vagotomy experiment, compared with the sham operation group, the sham + EA group showed a significant decrease in body weight, food intake, liver wet weight, adipose tissue wet weight (Pu0026lt;0.05). After gastric branch vagotomy, however, the regulatory effects of EA on body weight, food intake, liver wet weight, and other indicators were weakened. Similarly, after surgery EA did not exert a significant modulatory effect on the co-expression level of PGP9.5 and CGRP in the gastric antrum or on the expression of c-Fos-positive neurons in the NG. Conclusion Short-term HFD leads to desensitization of gastric vagal afferent signaling, manifested as impairment of local gastric vagal sensory nerves and a decrease in the number of activated neurons in the NG. EA can suppress food intake by repairing gastric vagal afferent signaling.

ObjectiveTo observe the role of leptin receptors （LepR） in the dorsal vagal complex （DVC） in electroacupuncture（EA） -mediated regulation of feeding behavior in obese mice， so as to elucidate its central mechanisms underlying improvement of metabolic disorders.Methods（1） Among wild-type （WT） mice， 10 were randomly selected as the normal group， and the remaining mice were fed with high-fat diet （HFD） to establish a obesity model. The successfully modeled mice were randomly divided into the HFD group and EA group， with 10 mice in each group. The EA group received EA stimulation （2 mA，2 Hz /15 Hz） at bilateral “Zusanli” （ST36） for 20 min， once daily， 6 times per week， for 5 weeks. The body weight， food intake， liver tissue wet weight， inguinal white adipose tissue （iWAT） weight， epididymal white adipose tissue （eWAT） weight， and brown adipose tissue （BAT） weight， and blood glucose levels were measured. The serum insulin and leptin contents were measured using ELISA. The gastric emptying rate was detected using phenol red meal method. Immunofluorescence staining was used to detect the co-expression of LepR-positive neurons and proto-oncogene c-Fos protein （c-Fos）， the expression of phosphorylated signal transducer and activator of transcription 3 （p-STAT3）， and the co-expression of choline acetyltransferase （ChAT） and c-Fos in the nucleus tractus solitarii （NTS） and dorsal motor nucleus of the vagus nerve （DMV）. （2） In addition， 10 leptin receptor knockout （LepR-/-） mice were randomly divided into LepR-/- normal group and LepR-/- EA group， with 5 mice in each group. The LepR-/- EA group received the same EA intervention as those described above. Gastric emptying rate was detected as that mentioned above.ResultsCompared with the WT normal group， the WT HFD group showed a significant increase in the body weight， liver and adipose （iWAT， eWAT and BAT） wet weight， serum insulin and leptin contents， fasting blood glucose level， and glucose tolerance area under the curve （AUC， all P<0.01）， and a considerable decrease in the gastric empty rate， the number of LepR and c-Fos co-expression neurons in the DMV and NTS， p-STAT3 positive and ChAT and c-Fos co-expression neuron expressions in the DMV （P<0.01， P<0.05）. In comparison with the model group， the body weight， food intake， liver and adipose wet weight， serum leptin content， fasting blood glucose， and glucose tolerance AUC were significantly decreased in the EA group （P<0.01）， while the gastric empty rate， number of LepR and c-Fos co-expression neurons in the DMV and NTS， p-STAT3 positive and ChAT and c-Fos co-expression neuron expressions in the DMV were notably increased in the EA group （P<0.01， P<0.05）. No significant differences were observed in the random blood glucose content and p-STAT3 positive neuron expression in the NTS after modeling and after EA and in the serum level of insulin after EA. （2） Compared with the WT normal group， the LepR-/- normal group showed an increase in gastric emptying rate （P<0.01）， while in comparison with the LepR-/- normal group， the LepR-/- EA group exhibited a decrease in gastric emptying rate （P<0.01）， suggesting an involvement of LepR in EA-induced enhancement of gastric emptying. There was a positive correlation between the gastric emptying rate and the number of LepR-positive neurons.ConclusionEA at ST36 can inhibit food intake and promote gastric empty to reduce body weight in obesity mice， which may be associated with its functions in increasing LepR expression in the DVC and restoring vagal central signaling.

Pancreatic nerves exhibit significant anatomical and functional disparities across species, with profound implications for metabolism and clinical practices like pancreatic transplantation and disease treatment. In humans, pancreatic nerves feature a complex distribution of sympathetic and parasympathetic fibers, forming intricate plexuses that closely interact with surrounding organs, playing a crucial role in regulating both endocrine (e.g., insulin and glucagon release) and exocrine secretions to maintain metabolic balance. Rodents, such as rats and mice-common experimental models-have relatively simpler pancreatic nerve architectures; for instance, mice show more concentrated nerve fibers around islets, while rats display greater variability in nerve density across pancreatic regions, which influences their responses to metabolic stimuli and makes them valuable but not fully analogous to human models. Canines and felines, often used in translational studies, possess pancreatic nerve systems that share some similarities with humans, such as comparable nerve plexus organization, yet differ in fiber type proportions, affecting their susceptibility to metabolic abnormalities like pancreatitis-related glucose dysregulation. These species-specific differences in pancreatic nerves directly impact metabolic processes: In humans, impaired nerve function is linked to metabolic disorders like diabetes and obesity, whereas in animal models, variations in neural control of hormone release and pancreatic homeostasis lead to differences in disease progression and response to interventions. Understanding these discrepancies is vital: It not only helps interpret findings from animal studies when translating to human therapies but also guides pancreatic transplantation by highlighting the need for species-specific considerations in nerve reconstruction to restore metabolic function, and identifies potential therapeutic targets tailored to the unique neural-metabolic interactions of each species.

This retrospective study assessed the impact of emotional factors on acupuncture efficacy in patients with overweight and hyperlipidemia, to guide the development of a more comprehensive and personalized treatment protocol. Using standardized acupuncture procedures, we analyzed data from 1,128 patients, categorizing them into groups with or without emotional abnormalities based on Hamilton Anxiety Rating Scale (HAMA) scores (cutoff ≥14). After 1:1 propensity score matching, 436 patients were included, with comparable baseline characteristics (all P > 0.05). Both groups showed significant improvements in primary outcomes, including body weight, BMI, obesity degree, total cholesterol, triglycerides, HDL-C, and LDL-C after treatment (P < 0.05). However, the group with emotional abnormalities exhibited less pronounced improvements in body weight, BMI, obesity degree, total cholesterol, and triglycerides compared to the normal emotion group (P < 0.05). These findings indicate that while acupuncture significantly improves clinical outcomes in these patients, emotional abnormalities reduce its therapeutic efficacy. Future acupuncture protocols for the overweight should incorporate emotional factors to optimize treatment outcomes.

Introduction: Simple obesity is an increasingly prevalent chronic condition. While electroacupuncture (EA) has demonstrated potential in addressing this issue, its effectiveness may be hindered by insufficient continuous stimulation and challenges related to patient adherence. This study aimed to compare the efficacy of EA alone versus EA combined with press needles in the treatment of simple obesity and to explore the underlying mechanisms contributing to weight loss. METHODS:Eighty simple obese patients with a body mass index (BMI) ≥25.0 kg/m2 were divided into two groups: the observation group (treated with EA combined with press needles) and the control group (treated with EA alone). The efficacy of the treatments was evaluated by monitoring obesity indicators. Additionally, obesity rat models were established through a high-fat diet (HFD), and rats were randomly assigned to three groups: obesity control group (no treatment), EA group, and EA combined with press needles group. Treatment outcomes were assessed by monitoring obesity indicators, examining adipose and liver cell morphology using staining techniques, and evaluating intestinal lymphatic vessel function through qRT-PCR, Western blot, and immunofluorescence analyses. RESULTS:The patients in the observation group exhibited significantly lower body weight (BW), BMI, body fat percentage (F%), abdominal circumference (A), waist circumference (WC), as well as serum levels of intestinal lymphatic function-related factors such as VEGF-C, delta-like ligand 4 (DLL4), and adrenomedullin (ADM) compared to the control group. Similarly, compared to EA group, EA combined with press needles significantly decreased obesity indexes, serum intestinal lymphatic function-related factors, and improved lymphatic vessel function in obese rats. Mechanistically, the VEGF-C/VEGFR-3/PI3K/AKT signaling pathway was inhibited by EA combined with press needles intervention. CONCLUSION:The combined therapy of EA with press needles had shown significantly superior efficacy in treating simple obesity compared to EA treatment alone. It achieved this by modulating the VEGF-C/VEGFR-3/PI3K/AKT signaling pathway, improving lymphatic vessel structure and function, and ultimately inhibiting obesity. .