Copyright: ©Author(s) 2026.
World J Diabetes. Nov 15, 2026; 17(11): 121630
Published online Nov 15, 2026. doi: 10.4239/wjd.121630
Published online Nov 15, 2026. doi: 10.4239/wjd.121630
Figure 4 Overexpression of gonadotropin-releasing hormone receptor sensitizes β-cells to gonadorelin-induced signaling.
A-C: Verification of gonadotropin-releasing hormone receptor (GnRHR) overexpression at the protein level following transfection with the plasmid cytomegalovirus-GnRHR plasmid in MIN6 cells; D-I: Representative immunoblots and corresponding densitometric analysis revealing the augmented phosphorylation of PKA and CREB, as well as the increased expression of PDX1, in GnRHR-overexpressing cells compared to empty vector controls upon gonadorelin stimulation. Data are expressed as the mean ± SEM (n = 3 independent biological replicates). aP < 0.05, bP < 0.01, cP < 0.001, and dP < 0.0001. pCMV: Plasmid cytomegalovirus; GnRHR: Gonadotropin-releasing hormone receptor.
- Citation: Dai XJ, Gao SC, Chen PT, Yang L, Kong CC, Ye CY, Xu ZX, Hu YX, He CY, Zuo ZH, Wang W. Postmenopausal high-gonadotropin-releasing hormone environment mediates pancreatic β-cell compensation via the cAMP-PKA-PDX1 pathway. World J Diabetes 2026; 17(11): 121630
- URL: https://www.wjgnet.com/1948-9358/full/v17/i11/121630.htm
- DOI: https://dx.doi.org/10.4239/wjd.121630