Cardiac myocyte-specific expression of beta3-adrenergic receptors sustains AMPK activation and glucose uptake while reducing hypertrophy following pressure overload

Cardiac beta3-adrenergic receptors (B3AR) produce effects antipathetic to those of B1 and B2 receptors. Importantly, B3AR are resistant to desensitization and their expression is upregulated in the diseased myocardium. We previously showed that mice with moderate cardiac-specific expression of the human B3AR (B3-TG) are protected from hypertrophy and fibrosis upon hemodynamic or neurohormonal stress. Here we tested the hypothesis that myocardial...