Objective To establish and evaluate a sterile golden hamster diabetes model by fecal microbiota transplantation(FMT). Methods Twenty-five male SPF-grade SD rats were divided into the control (SD-CN) group and the model (SD-DM) group, with 10 rats in the SD-CN group and 15 rats in the SD-DM group. After being fed with normal feed and high-fat feed respectively for 3 weeks, the animals were fasted for 12 h. In the SD-DM group,Streptozotocin (STZ) was intraperitoneally injected at a dose of 25 mg / kg for 3 consecutive days. Twenty-four male golden hamsters were divided into a control (CN) group and a model (DM) group (n= 12 hamsters per group), the fecal suspensions of SD rats in the SD-CN group and the SD-DM group were inoculated respectively. The animals were euthanized 10 weeks after FMT and blood and small intestine, pancreas, and large intestine contents were collected for blood biochemistry, histopathological examination, and 16S rRNA sequencing. Results After fecal microbiota transplantation, apolipoprotein A1 and apolipoprotein B levels differed significantly between the two groups ( P<0. 05). Glucagon and fasting blood glucose levels were significantly increased (P<0. 01) and fasting insulin was significantly decreased (P<0. 001) in the DM group, presenting obvious characteristics of glycolipid metabolism disorder and insulin resistance. Compared with that in the CN group, the pancreas in the DM group showed multifocal fat deposition, islet atrophy, reduced islet cells, irregular islet shape, swelling and necrosis, islet cell proliferation,increased capillaries, and thickening of the basement membrane, demonstrated by hematoxylin-eosin(HE) staining.Hamsters in the DM group showed hyperplasia of the small intestinal villus epithelium, fusion and disordered arrangement of small intestinal villi, cell swelling accompanied by degeneration and necrosis, and aggregation of inflammatory cells in the lamina lining of the small intestinal mucosa. 16S rRNA sequencing showed significant differences in intestinal microbiota diversity and the abundance of specific microbiota between the two groups. The chao1, shannon, and simpson indexes of α diversity were significantly decreased in the DM group (P<0. 05) and the unweighted Unifrac distance was significantly decreased (P<0. 01), suggesting differences in β diversity. The composition of the intestinal bacterial communities differed significantly between the two groups, with significantly increased Verrucomicrobiota ( P<0. 05) and significantly decreased Firmicutes in the DM group ( P<0. 05). Conclusions A sterile golden hamster diabetes model was successfully established using fecal microbiota transplantation technology. The animals presented with clinical characteristics similar to those of diabetes, thus providing an animal model for in-depth research on the relationship between the intestinal microbiota and the occurrence and development of diabetes.