Geniposide Balances the Redox Signaling to Mediate Glucose-Stimulated Insulin Secretion in Pancreatic β-Cells.

Abstract

PurposeTo investigate the effect of geniposide on the biosynthesis of insulin and the expression protein disulfide isomerase (PDI) and endoplasmic reticulum oxidoreductin 1 (ERO1) in the presence of low (5 mM) and high (25 mM) glucose in pancreatic β cells.MethodsThe content of insulin was measured by ELISA, the number of SH groups was determined with the classical chromogenic reagent, 5,5ʹ-dithiobis-(2-nitrobenzoic) acid (DTNB; also known as Ellman’s reagent), the expressions of PDI and ERO1 were analyzed by Western blot.ResultsGeniposide played contrary roles on the accumulation of H2O2, the ratio of GSH/GSSG and the thiol–disulfide balance in the presence of low (5 mM) and high (25 mM) glucose in rat pancreatic INS-1 cells. Geniposide also regulated the protein levels of protein disulfide isomerase (PDI) and endoplasmic reticulum oxidoreductin1 (ERO1), the two key enzymes for the production of H2O2 during the biosynthesis of insulin in INS-1 cells.ConclusionGeniposide affects glucose-stimulated insulin secretion by modulating the thiol–disulfide balance that is controlled by the redox signaling in pancreatic β cells.