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

Figure 3 Requirement of gonadotropin-releasing hormone receptor for gonadorelin-mediated signaling and insulin secretion. A-C: Validation of the knockdown efficiency of gonadotropin-releasing hormone receptor (GnRHR)-targeting small interfering RNA via western blotting in MIN6 cells; D: Effect of GnRHR silencing on the potentiation of insulin secretion by gonadorelin; E: Effect of GnRHR silencing on gonadorelin-induced intracellular cAMP production; F-I: Representative immunoblots and corresponding densitometric quantification demonstrating that GnRHR deficiency abolishes the gonadorelin-induced phosphorylation of PKA and CREB, as well as the upregulation of PDX1. Data are presented as the mean ± SEM (n = 3 independent biological replicates). ^aP < 0.05, ^bP < 0.01, and ^cP < 0.001. GnRHR: Gonadotropin-releasing hormone receptor.