Key result
Higher concentrations of palmitoyl-l-carnitine (10 μM) depolarized mitochondrial membrane potential, opened the mPTP, and increased ROS generation in rat ventricular myocytes.
Population
Saponin-treated rat ventricular myocytes
Comparison
Palmitoyl-l-carnitine and palmitoyl-CoA at… vs Baseline
Design
Preclinical
Authors
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Warrants no change in clinical lipotoxicity management; extends rat myocyte mechanistic data but leaves open human relevance.
Palmitoyl-l-carnitine and palmitoyl-CoA exert distinct detrimental effects on mitochondrial function in rat ventricular myocytes, providing mechanistic insights into cardiac lipotoxicity.
Tominaga et al. (2008) studied this question. Palmitoyl-l-carnitine and palmitoyl-CoA vs. baseline was evaluated on Membrane potential, opening of the mitochondrial permeability transition pore, and ROS production. Higher concentrations of palmitoyl-l-carnitine (10 μM) depolarized mitochondrial membrane potential, opened the mPTP, and increased ROS generation in rat ventricular myocytes.
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