Key result
Carvedilol (100 µmol/L) inhibited palmitate oxidation and increased glycolysis by nearly 50% in C2C12 cells, an effect likely related to alpha-1 adrenergic receptor blockade.
Carvedilol directly alters substrate metabolism in muscle cells by suppressing fatty acid oxidation and stimulating glycolysis, likely through alpha-1 adrenergic receptor blockade.
No takes yet. Share an insight, caveat, or question.
Carvedilol's metabolic shift in muscle cells warrants no practice change; leaves open in vivo cardiac relevance and mechanisms.
Onay-Beşi̇kçi̇ et al. (2012) studied this question. Carvedilol vs. Prazosin, propranolol, bisoprolol, or epinephrine was evaluated on Palmitic acid oxidation and glycolysis. Carvedilol (100 µmol/L) inhibited palmitate oxidation and increased glycolysis by nearly 50% in C2C12 cells, an effect likely related to alpha-1 adrenergic receptor blockade.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: