Electrical stimulated GLUT4 signalling attenuates critical illness-associated muscle wasting.

Alex B AddinsallNicola CaccianiAnders BackéusYvette HedströmGanna ShevchenkoJonas BergquistLars Larsson

Published in: Journal of cachexia, sarcopenia and muscle (2022)

ES maintained GLUT4 translocation through increased AMPK-TBC1D4 signalling leading to improved muscle glucose homeostasis. Soleus CSA and myosin content was promoted through reduced protein degradation via AMPK-FoxO3 E3 ligases, Atrogin-1 and MuRF1. These results demonstrate chronic supramaximal ES reduces critical care associated muscle wasting, preserved glucose signalling, and reduced muscle protein degradation in CIM.

Keyphrases

skeletal muscle
binding protein
protein protein
signaling pathway
blood glucose
metabolic syndrome
transcription factor
amino acid
adipose tissue
small molecule
cell proliferation
drug induced
glycemic control