miR-6835-3p regulates the function of pancreatic islet cells by modulating the expression of AdipoR1

Effective drugs and strategies for treating type 2 diabetes mellitus (2-DM) are urgently required. The aim of the present study was to elucidate the mechanism underlying microRNA (miR)-6835-3p regulation of adiponectin receptor 1 (AdipoR1) expression and the miR-6835-3p/AdipoR1 signaling pathway in pancreatic islet cells. In addition, the potential anti-diabetes effect of miR-6835-3p on insulin secretion was investigated. Luciferase activity analysis was performed to evaluate how miR-6835-3p targets the 3′-untranslated region of AdipoR1. The SU.86.86 and MIN-6 cell lines were co-cultured with or without miR-6835-3p inhibitors or mimics, and the insulin secretory functions of these cell lines were then determined. Luciferase reporter analysis revealed that AdipoR1 was a direct target of miR-6835-3p. In addition, miR-6835-3p overexpression suppressed the mRNA and protein expression levels of AdipoR1 in the SU.86.86 and MIN-6 cell lines. Furthermore, miR-6835-3p exerted negative effects on insulin secretion in SU.86.86 and MIN-6 cells, which were mediated by regulating AdipoR1 expression. AdipoR1 was a direct target of miR-6835-3p; therefore, inhibition of AdiopR1 expression may reduce insulin secretion and may be considered a key regulator of insulin secretion. The results of the present study suggested that targeting AdipoR1 with miR-6835-3p inhibitors may be a potential strategy for promoting glucose-stimulated insulin secretion, and thereby, may be an effective treatment for type 2-DM.