It has been proposed that the mechanism for myocardial triglyceride (TG) accumulation and diminished fatty acid oxidation in chronic alcoholic animals is mitochondrial damage and, possibly, altered palmitylcarnitine trasnferase (PCAT) activity. We have studied the fatty acid metabolism and PCAT activity of isolated heart mitochondria from 80 male rats pair-fed 52±7 days a liquid diet (35% fat) containing all essential nutrients but with ethanol or dextrin-maltose (control) as 36% of the total calories. Myocardial TG increased two to four times in alcohol-fed animals, but tissue free, acetyl- and acylcarnitine levels were unchanged. PCAT specific activity was not diminished in the alcoholic group (10.76±0.90 vs 13.38±1.60 nmol/min/mg) and Vmax and Km for carnitine were identical. Mitochondrial respiration rates with glutamate and palmityl- and acetylcarnitine were unchanged. However, pyruvate oxidation (states III and IV) in alcoholic animals was consistently reduced (200±23 and 28.3±4.0 vs 161±19 and 23.0±4.0 natoms oxygen/min/mg, respectively; P<0.001 and <0.02). These findings show that fat accumulation occurs despite the normal ability of the myocardium to transport and oxidize fatty acid. Furthermore, pyruvate dehydrogenase inhibition may be an early marker of alcohol induced myocardial damage.
- Alcoholic cardiomyopathy
- Fatty acid metabolism
- Palmityl carnitine transferase
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine