Insulin-like growth factor-1 activates AMPK to augment mitochondrial function and correct neuronal metabolism in sensory neurons in type 1 diabetes

Mohamad-Reza Aghanoori, Darrell R. Smith, Shiva Shariati-Ievari, Andrew Ajisebutu, Annee Nguyen, Fiona Desmond, Carlos H.A. Jesus, Xiajun Zhou, Nigel A. Calcutt, Michel Aliani, Paul Fernyhough
2019 Molecular Metabolism  
Diabetic sensorimotor polyneuropathy (DSPN) affects approximately half of diabetic patients leading to significant morbidity. There is impaired neurotrophic growth factor signaling, AMP-activated protein kinase (AMPK) activity and mitochondrial function in dorsal root ganglia (DRG) of animal models of type 1 and type 2 diabetes. We hypothesized that sub-optimal insulin-like growth factor 1 (IGF-1) signaling in diabetes drives loss of AMPK activity and mitochondrial function, both contributing to development of DSPN.
doi:10.1016/j.molmet.2018.11.008 pmid:30545741 pmcid:PMC6358538 fatcat:nwf6uihghveulgbmuuvppsswty