Glucose clearance and uptake is increased in the SOD1G93A mouse model of amyotrophic lateral sclerosis through an insulin-independent mechanism
T. S. McDonald, V. Kumar, J. N. Fung, T. M. Woodruff, J. D. Lee
This study shows that SOD1G93A mice exhibit increased glucose uptake and altered glucose homeostasis through an insulin-independent mechanism and impaired glucagon signaling in ALS.
bioRxiv · Aug 2, 2020Physiology