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Yagi et al (84) demonstrated that GCG promoted the proliferation of HT29, SW480, CT26 and CMT93 cells through GCGR-dependent AMPK deactivation and MAPK activation, using 1.0 nM GCG replenished every 24 h for up to 72 h

showed a small, albeit statistically significant, increase in HbA1c in one long-term study, while no effect was observed in another long-term study and no significant effects were noted in short-term studies among patients with non-diabetic peripheral neuropathic pain [164]

The protein expression of LC3II/LC3I and P62 altered in a similar manner (Fig

Notably, the majority of mechanistic data supporting this concentration-dependent model derives from preclinical studies using mouse pancreatic -cells and clonal cell lines, with limited validation in human islet studies, necessitating further clinical investigation to confirm these concentration thresholds in human diabetes treatment [23,24,25,26]