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.