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

Figure 6 Gonadorelin potentiates glucose-stimulated insulin secretion in MIN6 cells. A: Dose-response analysis of gonadorelin-mediated insulin secretion under hyperglycemic conditions (16.7 mmol/L glucose); B: Comparison of absolute insulin release levels, demonstrating the synergistic effect of gonadorelin on basal glucose-stimulated insulin secretion; C: Pharmacological inhibition of the gonadorelin-mediated insulinotropic effect by the specific gonadotropin-releasing hormone receptor antagonist cetrorelix; D-H: Representative immunoblots and corresponding densitometric quantification of the phosphorylation and expression of signaling effectors (PKA, CREB1, and PDX1) under high-glucose conditions. Statistical analysis: Data are expressed as the mean ± SEM (n = 3 independent biological replicates). Statistical significance was determined using one-way ANOVA, followed by Tukey’s post hoc test. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, and ^dP < 0.0001.