Objective: To explore the mechanism of action of vitamin D in regulating autophagy activity and improving type 2 diabetes in rats through the FXR/FGF15 signaling pathway.Methods: 40 SPF-grade SD rats were selected. Among them, 10 rats were set as the control group, and 30 were used to establish the type 2 diabetes model. The 27 successfully modeled rats were divided into a model group, a vitamin D group, and a vitamin D + FXR inhibitor group, with 9 rats in each group. The histopathological changes in renal tissue, fasting blood glucose, insulin, body weight, renal function, inflammatory factor levels, autophagy-related proteins, and mRNA and protein expression levels of the FXR/FGF15 pathway in rats from each group were compared.Results: The renal tissue structure of rats in the control group was normal. In the model group, the rats exhibited glomerular hypertrophy, mesangial cell proliferation, and swelling, degeneration, and partial atrophy of renal tubular epithelial cells. The renal pathological damage in the vitamin D group was alleviated, while the damage in the vitamin D + FXR inhibitor group was more severe than that in the vitamin D group, with a degree between that of the model group and the vitamin D group. Compared with the control group, the model group rats exhibited elevated fasting blood glucose, creatinine (Scr), blood urea nitrogen (BUN), monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and P62 protein expression. The mRNA and protein expression levels of insulin, body mass, lysosomal-associated membrane protein 1 (LAMP1), LC3-II/I protein, farnesoid X receptor (FXR), and fibroblast growth factor 15 (FGF15) decreased, with statistically significant differences (P < 0.05). Compared with the model group, the vitamin D group exhibited reduced fasting blood glucose, Scr, BUN, MCP-1, IL-6, IL-1β, TNF-α, and P62 protein expression, while insulin, body weight, LAMP1, LC3-II/I protein, FXR, FGF15 mRNA, and protein expression levels were increased (P < 0.05). Compared with the vitamin D group, the rats in the vitamin D + FXR inhibitor group exhibited increased fasting blood glucose, Scr, BUN, MCP-1, IL-6, IL-1β, TNF-α, and P62 protein expression, and decreased insulin, body weight, LAMP1, LC3-II/I protein, FXR, FGF15 mRNA, and protein expression levels, with statistically significant differences (P < 0.05). Conclusion: Vitamin D can improve renal function, and its mechanism of action may be related to regulating autophagy activity and the FXR/FGF15 pathway.