Presentation description

With a globally aging population, the need for treatments that address age related comorbidities are more relevant than ever. Previous research done in our lab has shown that treatment of mice with the compound N-Acetyl-Carnosine (N-Ac-Carn) could partially prevent protein damage caused by lipid peroxidation, and subsequent muscle atrophy and weakness in a mouse-model of inactivity. N-Ac-Carn is endogenously produced, safe, and affordable making it a potentially promising strategy for age-related functional decline. Our current pre-clinical trial aims to comprehensively determine the efficacy of N-Ac-Carn treatment in preventing age-related functional decline. To this end, 18-month-old mice were treated with either normal water (CON) or water supplemented with 80mM N-Ac-Carn (N-Ac-Carn) for 6 months. Targeted metabolomics verified that this treatment enriched all tissues with N-Ac-Carn. Mice treated with N-Ac-Carn maintained higher body weights longer than CON (Interaction: p=0.022). This effect was driven specifically by higher fat mass over time (p=0.016) in female mice. These changes in the N Acetyl Carnosine mice were not explained by an increase in overall food consumption, which remained similar across both groups. Metabolic cage analysis revealed lower VO2 in N-Ac-Carn mice (Group: p=0.002) although this effect was observed in both male and female mice (Interaction: p=0.878). Despite higher fat mass, IPGTT revealed equivocal glucose tolerance in CON and N-Ac-Carn mice. Therefore, this preserved fat mass with aging is not detrimental to metabolic regulation and may be protective against developing other symptoms of frailty. Future analysis will pursue the mechanisms of preserved adipose tissue mass with N-Ac-Carn treatment and if this phenotype is associated with improved health span.