Objective: The Goto-Kakizaki (GK) rat is a well-studied model of the non-obese spontaneous type 2 diabetes with impaired glucose-stimulated insulin secretion as one of the main associated disease phenotypes. MicroRNAs (miRNA) are small non-coding RNAs which have been implicated in insulin secretion in beta cells. We aim to detect glucose-regulated miRNAs in the GK islets involved in the disease and identify targets via correlation with mRNA expression data. Methods: Expression of 350 known rodent miRNAs were profiled for GK and control Wistar rats using a locked-nucleic acid-based array (n=6 per group, 60 days old, female). Stem- loop RT qPCR was used to validate differentially- regulated miRNAs. MiRNA expression trajectories were determined in islets incubated in different glucose concentrations. Predicted targets of glucose-regulated miRNAs were filtered using published mRNA expression data. Gene enrichment analysis was performed to identify associated gene ontology (GO) categories. Results: We identified the predominance of 24 upregulated miRNAs in the GK pancreatic islets. The expression trajectories of qPCR-validated GK miRNAs in 2.8 mM, 8.3 mM and 16.7 mM glucose diverged from the control Wistar miRNAs both in magnitude and direction. Forty-six glucose-regulated targets were filtered out of combined bioinformatics target prediction and mRNA data, showing enrichment for genes with known roles in beta cell exocytosis, notably granuphilin and SNAP-25. Conclusion: We identified glucose-regulated miRNAs significantly upregulated in the GK pancreatic islets. Filtering of predicted targets by mRNA expression data generated a set of genes involved in beta cell exocytosis. Our results support the notion that impaired miRNA regulation of targets involved in insulin secretion contributes to the GK diabetic phenotype.