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. 2015 Mar;156(3):1156–1170. doi: 10.1210/en.2014-1619

Figure 8.

Figure 8.

Illustration of the working mechanisms for FGF21 prevention of spontaneous and diabetes-induced germ cell apoptosis. Diabetes adversely affects glucose metabolism (AKT/GSK-3β/GS signaling) and fatty acid oxidation (AMPK/Sirt1/PGC-1α) in testis, leading to the accumulation of metabolic intermediates that cause testicular oxidative damage and germ cell apoptosis. FGF21 deficiency exacerbates these defects, leading to testicular cell apoptosis. In nondiabetics, FGF21 preserves almost normal spermatogenesis through the AKT-signaling pathway to inhibit p53 via AKT1/MDM2.