Postmenopausal high-gonadotropin-releasing hormone environment mediates pancreatic β-cell compensation via the cAMP-PKA-PDX1 pathway

Figure 2 Gonadorelin promotes basal insulin secretion by activating the gonadotropin-releasing hormone receptor-cAMP-PKA-PDX1 signaling axis. A: Dose-dependent effects of gonadorelin on insulin secretion in MIN6 cells under basal glucose conditions (2.8 mmol/L); B and C: Antagonism of the insulinotropic effect of gonadorelin by the specific gonadotropin-releasing hormone receptor antagonist cetrorelix; D: Intracellular cAMP levels in MIN6 cells stimulated with gonadorelin in the presence or absence of cetrorelix; E-H: Representative immunoblots and densitometric analysis of the expression and phosphorylation levels of PKA, CREB, and PDX1. β-actin was utilized as the loading control. Statistical analysis: Data are presented as the mean ± SEM (n = 3 independent experiments). ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, and ^dP < 0.0001. GnRH: Gonadotropin-releasing hormone.