Effect of thyroxine treatment on exogenous myocardial lactate oxidation.
The effect of thyroxine treatment on myocardial lactate oxidation was examined by use of an isolated, working rat heart preparation. Thyroxine treatment, both acute and chronic, was associated with a decrease in lactate oxidation, when the heart was perfused with a physiological blend of substrates (free fatty acids, lactate, and glucose). This decrease in lactate oxidation was not caused by a generalized impairment in mitochondrial oxidation of acetyl coenzyme A (CoA), as oxygen consumption was normal and fatty acid oxidation was elevated in the treated animals. The block in lactate oxidation was localized to the conversion of pyruvate to acetyl CoA, as indicated by the depressed oxidation of pyruvate and lactate. Thyroxine treatment was associated with a decrease in pyruvate dehydrogenase activity. The decrease in pyruvate dehydrogenase activity was reversible and was attributed to the enhanced myocardial oxidation of free fatty acids.
D000818:Animals; D001835:Body Weight / Q000187:drug effects; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects; D007773:Lactates / Q000378:metabolism*; D019344:Lactic Acid; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009929:Organ Size / Q000187:drug effects; D010084:Oxidation-Reduction; D010101:Oxygen Consumption / Q000187:drug effects; D019308:Palmitic Acid; D010169:Palmitic Acids / Q000378:metabolism; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013974:Thyroxine / Q000494:pharmacology*
D007773:Lactates; D010169:Palmitic Acids; D011768:Pyruvate Dehydrogenase Complex; D019308:Palmitic Acid; D019344:Lactic Acid; D013974:Thyroxine