Cardiac hypertrophy in sarcopenic obese C57BL/6J mice is independent of Akt/mTOR cellular signaling

Sarcopenic obesity (SO) is the comorbidity of age-related muscle wasting and obesity. SO increases the risk of heart disease, but little is known about the cellular signaling in cardiac muscle of SO individuals. Aim: The purpose of this study was to identify key cellular signaling alterations in cardiac muscle of sarcopenic obese mice. Methods: Thirty-two, male C57BL/6J mice were randomly divided into lean and high-fat fed groups and raised to 3-4 months (young) or 20-22 months (aged) of age. Hearts were extracted and processed for Western blot and qRT-PCR analyses. Results: Hearts of SO mice were 36-55% heavier than the young, obese or aged, lean groups. Markers downstream of Akt were not elevated in the SO group. p-p38:p38 MAPK was higher with age, and a 2-fold increase was observed in the obese vs. lean aged groups. pERK1/2:ERK1/2 MAPK was similar to 50-70% lower in the SO cardiac muscle compared to the young, obese group. pAMPK:AMPK was 50%-66% lower in the SO cardiac muscle compared to the obese and lean, aged groups. mRNA abundance of TNF alpha was similar to 2.5-fold higher in the SO group. Conclusion: Cardiac hypertrophy in SO is likely pathogenic as evidenced by the alterations in MAPK and AMPK protein content and lack of activation in the Akt/mTOR pathway.