Objective: Our study aimed to investigate the mechanism by which miR-217 regulates pancreatic beta cell functions by targeting the KRAS gene in type 2 diabetic mice. Methods: We used a dual luciferase reporter assay to confirm that KRAS is a target to which miR-217 binds. HE staining was used to observe the morphology of the islets. The fasting blood glucose levels (FBG), fasting insulin levels (FINS), and the homeostatic model assessment for insulin resistance (HOMA-IR) levels were measured. The cell proliferation and apoptosis were compared. qRT-PCR and Western blot were applied to measure the mRNA and protein expressions. Results: The fasting blood glucose levels (FBG), fasting insulin levels (FINS), and homeostatic model assessment for insulin resistance (HOMA-IR) levels were significantly increased in the type 2 diabetic model mice compared with the levels in the control mice. However, if the diabetic model mice were transfected with a miR-217 inhibitor and/or the KRAS overexpression plasmid pcDNA3.0-KRAS, the increases in the FBG, FINS, and HOMA-IR levels could be reversed. Regarding the in vitro transfections, the beta cells harvested from the type 2 diabetic model mice exhibited decreased cell viability and increased apoptosis. In addition, the expression of miR-217 was upregulated, and KRAS was downregulated. Transfection with either the miR-217 inhibitor or with pcDNA3.0-KRAS increased beta cell viability and decreased apoptosis. Co-transfection with the miR-217 inhibitor and pcDNA3.0-KRAS further enhanced these effects on the beta cells. Conclusion: miR-217 silencing promotes pancreatic beta cell proliferation and inhibits beta cell apoptosis by upregulating KRAS expression, and this outcome is conducive to the alleviation of insulin resistance in type 2 diabetic model mice.