Effects Of Long-Chain Non-Coding Rna-Small Nucleolar Rna Host Gene 1 (Snhg1) On Islet Beta Cell Activity And Insulin Secretion In High Glucose Environment Through Protein Kinase B (Akt)/The Mammalian Target Of Rapamycin (Mtor)/Glucose Transporter 2 (Glut2) Signaling Pathway

The pathogenesis of diabetes is closely related to islet beta-cell dysfunction. LncRNA-SNHG1 participates in various diseases. However, LncRNA-SNHG1's effect on islet beta-cell dysfunction in high glucose environment is unclear. The islet p-cell MIN6 cells were assigned into control group, high glucose group, and SNHG1 group (Lnc-SNHG1 plasmid was transfected into MIN6 cells in high glucose environment), followed by analysis of Lnc-SNHG1 expression by Real time PCR, insulin secretion levels, cell proliferation by MTT assay, Caspase 3 activity, Akt/mTOR/GLUT2 signaling pathway protein expression by western blot, glucose enzyme (GK) content by Real time PCR, as well as Pyruvate dehydrogenase (PDH) and GK activity. LncRNA-SNHG1 expression was decreased in high glucose environment, which inhibited cell proliferation, increased Caspase 3 activity, decreased insulin secretion and downregulated Akt, mTOR and GLUT2, as well as reduced GK content, PDH and GK activity with statistically significant differences compared to control (P < 0.05); LncRNA-SNHG1 plasmid transfection in high glucose environment MIN6 cells can significantly promote SNHG1 expression and cell proliferation, decrease Caspase 3 activity, increase insulin secretion and the expression of Akt, mTOR and GLUT2, elevate GK content and activity of PDH and GK (P < 0.05). LncRNA-SNHG1 expression is reduced in high glucose environments. Overexpression of LncRNA-SNHG1 in high glucose environment MIN6 cells up-regulated GLUT2 expression via Akt/mTOR signaling pathway, thereby promoting islet beta-cell function and insulin secretion.