Propionyl L-carnitine improvement of hypertrophied heart function is accompanied by an increase in carbohydrate oxidation.

doi:10.1161/01.RES.77.4.726

Paper

Propionyl L-carnitine improvement of hypertrophied heart function is accompanied by an increase in carbohydrate oxidation.

Published Oct 1, 1995 · B. Schönekess, Michael F. Allard, G. Lopaschuk

Circulation research

Q1 SJR score

100

Citations

2

Influential Citations

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Abstract

Propionyl L-carnitine (PLC) is a naturally occurring derivative of L-carnitine that can improve hemodynamic function of hypertrophied rat hearts. The mechanism(s) responsible for the beneficial effects of PLC is not known, although improvement of myocardial energy metabolism has been suggested. In this study, we determined the effect of PLC on carbohydrate and fatty acid metabolism in hypertrophied rat hearts. Myocardial hypertrophy was produced by partial occlusion of the suprarenal aorta of juvenile rats. Over a subsequent 8-week period, a mild hypertrophy developed, resulting in a 17% increase in heart weight in these animals compared with the sham-operated control animals. Myocardial carnitine was decreased in hypertrophied hearts compared with hearts from sham-operated animals (4155 +/- 383 versus 5924 +/- 570 nmol.g dry wt-1, respectively; P < or = .05). Perfusion of isolated working hearts for 60 minutes with buffer containing 1 mmol/L PLC increased carnitine content in hypertrophied hearts from 4155 +/- 383 to 7081 +/- 729 nmol.g dry wt-1 (P < or = .05). In the presence of 1.2 mmol/L palmitate, fatty acid oxidation rates were not decreased in the hypertrophied hearts compared with control hearts. PLC treatment did not alter rates of fatty acid oxidation in control hearts but did result in a small increase in rates in the hypertrophied hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

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Propionyl L-carnitine improves heart function in hypertrophied rats by increasing carnitine content and slightly increasing fatty acid oxidation rates.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Propionyl L-carnitine improvement of hypertrophied heart function is accompanied by an increase in carbohydrate oxidation.

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References

Fatty acid oxidation and cardiac function in the sodium pivalate model of secondary carnitine deficiency.

Carnitine deficiency in rats leads to depressed cardiac function and fatty acid oxidation, but glucose oxidation rates remain slightly increased.

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Hypertrophied hearts have a reduced contribution of fatty acid oxidation to energy production, but compensate by increasing glycolysis during low work conditions.

Propionyl-L-carnitine prevents myocardial mechanical alterations due to pressure overload in rats.

Propionyl-L-carnitine prevents myocardial mechanical alterations due to pressure overload in rats, maintaining muscle mechanics and ventricular wall composition independently of tissue carnitine levels.

Stunned myocardium after rapid correction of acidosis. Increased oxygen cost of contractility and the role of the Na(+)-H+ exchange system.

Rapid recovery of pH paradoxically depresses myocardial contractility and increases the oxygen cost of contractility, likely due to activation of the Na(+)-H+ exchange system.

Control of oxidative metabolism in volume-overloaded rat hearts: effects of different lipid substrates.

Using octanoate as a lipid substrate can protect ATP synthesis in volume-overloaded hearts, preventing contractile failure.

Citations

Afterload-induced Decreases in Fatty Acid Oxidation Develop Independently of Increased Glucose Utilization

Cardiomyocytes do not compensate for a deficit in glucose utilization by up-regulating fatty acid oxidation, even when glucose utilization is reduced.

Regulation of H9C2 cell hypertrophy by 14-3-3η via inhibiting glycolysis

14-3-3 can suppress cardiomyocyte hypertrophy by decreasing YAP expression and glycolysis, making it a promising target for inhibiting cardiac hypertrophy.

Cadmium contributes to cardiac metabolic disruption by activating endothelial HIF1A-GLUT1 axis.

Cadmium exposure disrupts cardiac metabolism by activating the endothelial HIF1A-GLUT1 axis, and inhibiting HIF1A could potentially improve cardiac metabolic disorders and Cd-related cardiovascular diseases.

Integrated Control of Fatty Acid Metabolism in Heart Failure

Disrupted fatty acid metabolism contributes to heart failure, and understanding its regulation may lead to promising new therapeutic targets.

The Effect of L- Carnitine on Cardiac Output in Patient with Chronic Kidney Disease on Regular Hemodialysis

L-carnitine supplementation in a suitable dose improves cardiac performance in patients with chronic kidney disease on regular hemodialysis.

Cardiac Energy Metabolism in Heart Failure

Cardiac energy metabolism alterations contribute to heart failure severity, with pharmacological targeting of these pathways potentially improving cardiac efficiency and function.

Hyperpolarized magnetic resonance shows that the anti‐ischemic drug meldonium leads to increased flux through pyruvate dehydrogenase in vivo resulting in improved post‐ischemic function in the diabetic heart

Meldonium improves pyruvate dehydrogenase flux in the diabetic heart, leading to improved cardiac recovery after ischemia.

Effect of Levocarnitine vs Placebo as an Adjunctive Treatment for Septic Shock

Levocarnitine did not meaningfully reduce organ failure at 48 hours in patients with septic shock.