Key result
Hereditary myocardiopathy in hamsters features depressed phosphorus uptake and enhanced glycolysis despite normal oxygen uptake.
Why the study?
Biochemical alterations in oxidative phosphorylation in hereditary fatal myocardiopathy and muscular dystrophy in hamsters were investigated to understand their relation to heart mechanical failure.
Answers are grounded in this paper and cite their sources.
Biochemical studies have been performed on the hearts of hamsters afflicted with a hereditary, fatal myocardiopathy and muscular dystrophy. In sarcosomes from myopathic hearts phosphorus uptake and phosphorus/oxygen ratios were depressed, while oxygen uptake was normal. The enhanced rate of glycolysis in slices from myopathic hearts could be explained by changes in high energy phosphate compound metabolism. The relationship between the biochemical changes and the mechanical failure of the heart is discussed.
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Lochner et al. (1968) studied Hereditary myocardiopathy and muscular dystrophy. Hereditary myocardiopathy vs. Normal hearts (implied) was evaluated on Phosphorus uptake, phosphorus/oxygen ratios, oxygen uptake, and glycolysis rate. In Syrian hamsters with hereditary myocardiopathy, sarcosomal phosphorus uptake and phosphorus/oxygen ratios were depressed while oxygen uptake was normal, alongside an enhanced rate of glycolysis.
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