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.

OBJECTIVE

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 ~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 TNFα was ~2.5-fold higher in the SO group.

CONCLUSIONS

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.