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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
Molecular metabolism | 2019

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.

Pubmed ID: 30545741

Research resources used in this publication

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Associated grants

  • Agency: NINDS NIH HHS, United States
    Id: R01 NS081082
  • Agency: NIDDK NIH HHS, United States
    Id: DP3 DK108245
  • Agency: CIHR, Canada
    Id: MOP-130282

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