Metabolic changes in the myocardium of hamsters with hereditary muscular dystrophy.
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Depressed fatty acid (FA) oxidation found previously in various types of cardiomyopathies has been attributed to the lack of carnitine in heart muscle. This is not the case in the cardiac lesion of hamsters, strain BIO 14.6, between the ages of 3 and 6 months. We observed depressed CO2 production by heart homogenates of diseased animals from labeled acetate (1/20), butyrate (1/15), octanoate (1/3, and palmitate (1/4) in the presence of carnitine. The activity of carnitine palmitoyltransferase (forward reaction) and FA activating enzymes was unchanged. The oxidation of 1,4-labeled succinate as well as acetyl CoA was depressed to approximately 40% of the control, whereas [2-14C]pyruvate and [U-14C]oxoglutarate were oxidized at 60 to 70% of the control level. The CO2 production from [1-14C]pyruvate and [1-14C]oxoglutarate showed no reduction. No significant difference was found in myocardial triglyceride content and palmitate esterification into neutral lipids. The possible cause of different magnitudes of depressed oxidation of these substrates is unknown. It may be that the acetyl-CoA derived from FAs and that derived from pyruvate are metabolized by the TCA cycle to different extents, or that the endogenous metabolism participates to different degrees in the presence of different substrates.
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