Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.02.233411v1?rss=1 Authors: McDonald, T. S., Kumar, V., Fung, J. N., Woodruff, T. M., Lee, J. D. Abstract: Metabolic disturbances are associated with the progression of the neurodegenerative disorder, amyotrophic lateral sclerosis (ALS). In this study we aimed to elucidate deficits in energy homeostasis in the SOD1G93A mouse model of ALS and tissue specific changes in the periphery that underlie these perturbations. We found that at the mid-symptomatic stage of disease, SOD1G93A mice had an increase in oxygen consumption, and faster exogenous glucose uptake, despite no change in insulin sensitivity. Fasting glucose homeostasis was disturbed, along with changed concentrations in the glucoregulatory hormones, insulin and glucagon. Finally, the metabolic gene expression profile in the liver of SOD1G93A mice, and increase in glycogen stores indicate that glucose cannot be utilised efficiently. Overall, we found that glucose homeostasis and uptake is altered in SOD1G93A mice at the mid-symptomatic stage, potentially due to the increase in insulin-independent glucose uptake and disturbance in glucagon sensitivity. Copy rights belong to original authors. Visit the link for more info