Table 5:

Role of miRNAs in diabetes.

miRNA	Models Used	Function	References
miR-375	MIN6, Nit-1, INS1E	Inhibits GSIS by targeting Mtpn and blocking the fusion and exocytosis of insuiln vesicles at β-cell membrane; also possibly downregulates NF-κB activity. Reduces insulin production and β-cell proliferation by targeting PDK1 and inhibiting PI3K signaling axis	58, 82
miR-124a	MIN6	Increases basal insuline secretion but decreases GSIS by upregulating SNAP25, Rab3A, and synapsin-1A while decreasing Rab27A and Noc2. Rab27A is a direct target.	79
miR-96	MIN6	Inhibits GSIS by upregulating the expression of granuphilin and decreasing Noc2 levels	79
miR-145	MIN6	Decreases GSIS by targeting ABCA1 and decreasing the efflux of cholesterol from the β-cell	81
miR-33	MIN6	Decreases GSIS by targeting ABCA1 and causing accumulation of cholesterol in the β-cell	80
miR-7	MIN6	Negative regulator of GSIS by directly regulating genes involved in distal stages of the fusion of the insulin vesicle with cell membrane and interaction with ternary SNARE complex.	62
miR-204	INS-1, MIN6	Downregulates insulin transcription by directly targeting insulin transcription factor MAFA. Also decreases insulin secretion by targeting GLP1R.	83, 84
miR-21	INS-1, MIN6	Promotes β-cell proliferation. Overexpression increases β-cell proliferation but also activates apoptosis, impairing net β-cell survival. Also downregulates GSIS via indirect inhibition of VAMP2 but does not affect basal insulin secretion	85, 86
miR-34a	INS-1, MIN6	Promotes β-cell death by downregulating SIRT1 and enhancing p53-mediated apoptosis	85, 86
miR-200	MIN5, INS-1E	Contributes to β-cell apoptosis by downregulating antiapoptotic and stress-resistance pathways. Also activates Trp53 pathway and concomitant expression of pro-apoptotic genes.	87