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

Figure 8 Gonadotropin-releasing hormone-associated compensatory signaling is limited by islet structural deterioration in advanced diabetes. A-D: Representative immunoblots and densitometric quantification of PKA, CREB1, and PDX1 in isolated islets; E: Representative hematoxylin and eosin staining of pancreatic sections; arrowheads denote islet atrophy and structural disarray in diabetic cohorts (scale bars: 100 μm and 50 μm). F and G: Quantitative analysis of mean islet area (F) and total islet number (G); H: Β-to-α cell area ratio; I: Dual-immunofluorescence staining for insulin (red) and glucagon (green). Nuclei were counterstained with DAPI (blue). Scale bar: 200 μm. Data are expressed as the mean ± SEM (n = 8-10 animals per group). ^aP < 0.05, ^bP < 0.01, and ^dP < 0.0001. OVX: Ovariectomy.