This study investigated whether electroacupuncture (EA) can improve glucose and lipid metabolism and obesity in mice via activation of intestinal FXR‑mediated signaling pathways, specifically the FXR/TGR5/GLP‑1 axis and the FXR/FGF15 pathway. The work used a high‑fat diet to induce obesity in male C57BL/6 mice and evaluated metabolic, histological, and molecular endpoints in ileal tissue.
Fifty specific pathogen‑free (SPF) male C57BL/6 mice were enrolled. Animals were randomized into a blank (control) group (n = 8) and a pre‑model group (n = 42). Obesity was induced in the pre‑model animals using a high‑fat diet. From the obese cohort, 24 mice were further randomized into three groups (n = 8 per group): a model group (obese, no intervention), an EA group, and a sham EA group.
In the EA group, bilateral acupoints Zusanli (ST36) and Tianshu (ST25) were stimulated with electroacupuncture for 30 minutes per session. Interventions were administered once every other day, three times per week, for four weeks. The sham EA group received shallow subcutaneous needling at ST36 and ST25 and had the EA instrument connected but without applied electrical stimulation.
The investigators recorded body weight and Lee’s index before and after the intervention period. Serum biochemical measures included triglyceride (TG), total cholesterol (TC), low‑density lipoprotein cholesterol (LDL‑C), fasting blood glucose (FBG), and fasting insulin (FINS). Insulin resistance was estimated using the homeostatic model assessment index (HOMA‑IR). Intestinal morphology was evaluated by hematoxylin and eosin (HE) staining of ileal tissue to assess mucosal damage and inflammatory infiltration.
Expression levels of FXR, TGR5, GLP‑1, and FGF15 in ileal tissue were measured at both the protein and mRNA levels. Protein expression was assessed by Western blot and mRNA levels by fluorescence quantitative PCR (qPCR).
Compared with the blank (control) group, the high‑fat diet model group showed significant metabolic deterioration: increased body weight and Lee’s index, elevated serum TG, TC, LDL‑C, higher FBG and FINS, and increased HOMA‑IR (all reported P < 0.01). Histologically, ileal mucosal tissue in model mice was substantially damaged with epithelial cell loss, disordered arrangement, and stromal inflammatory cell infiltration. Molecularly, ileal protein and mRNA expression of FXR, TGR5, GLP‑1, and FGF15 were significantly decreased in the model group compared with blank (P < 0.01).
Relative to the model group, both the EA and sham EA groups had decreased body weight (P < 0.01). The EA group specifically demonstrated reductions in Lee’s index, serum TG, TC, LDL‑C, FBG, FINS, and HOMA‑IR (P < 0.01). Ileal pathology was notably less severe after EA, and the EA group showed significant increases in ileal FXR, TGR5, GLP‑1, and FGF15 protein and mRNA expression (all reported P < 0.01).
The abstract reports that the expression level of T… (text truncated). The final comparative details for the sham EA group’s molecular expression were not fully reported in the source abstract; therefore specific differences between sham EA and model or EA groups for every molecular marker cannot be stated beyond what is provided.
The authors conclude that EA at ST36 and ST25 ameliorated metabolic dysfunction, improved ileal histology, and upregulated intestinal FXR‑related signaling (including TGR5, GLP‑1, and FGF15) in high‑fat diet–induced obese mice. These findings support a mechanism in which intestinal FXR‑mediated pathways contribute to EA’s beneficial effects on glucose and lipid metabolism in this animal model.
Limitations based on the available source text: the abstract provided is truncated and does not include full comparative data for the sham EA group at the molecular level, numerical values for biochemical and molecular endpoints, or detailed statistical methods beyond P‑value thresholds. Additional methodological details, effect sizes, and full results tables were not reported in the provided abstract and would require consultation of the full text for complete evaluation.
Overall, the study presents preclinical evidence that EA can modulate intestinal nuclear receptor and enteroendocrine signaling associated with metabolic regulation in obese mice, but full appraisal requires the complete article for quantitative outcomes, statistical analyses, and any discussion of safety or translational considerations.