Transcriptomic alteration of SOD1-G93A mutation and leptin deficiency in the adipose tissue

Amyotrophic lateral sclerosis (ALS) is a multifactorial and complex fatal degenerative disorder. Both patients and animal models have significant dysregulation in metabolism that can be associated with body weight loss and hypermetabolism. A higher body mass index appears to have protective effects on the disease, but the role of adipose tissue is still not well understood. In this work we have proposed the following objectives: a) determine the effects that the SOD1G93A mutation has on adipose tissue b) study how an increase in body mass through a genetic deficiency in leptin impacts in the adipose tissue of mice SOD1G93A. To investigate the effects of SOD1G93A mutation and leptin deficiency on the adipose tissue , the iWAT depots of WT, Lepob/+, SOD1G93A, SOD1G93A-Lepob/+ female mice, was dissected at 90 days of age, and the RNA was isolated to perform the bulk RNA-sequencing study (n=4 per group).