Why the study?
Does chronic ethanol feeding alter subcellular protein fractions and synthesis rates in the hearts of young rats?
Does chronic ethanol feeding alter subcellular protein fractions and synthesis rates in the hearts of young rats?
Chronic ethanol feeding in rats reduces myofibrillar protein content despite increased synthesis rates, suggesting independent regulation that may contribute to alcoholic cardiomyopathy.
Indicates dissociation of myofibrillar synthesis from content in ethanol-exposed rat hearts; leaves open relevance to human alcoholic cardiomyopathy.
An investigation was made into the chronic effects of ethanol on the subcellular protein fractions in the hearts of young rats (80-100 g body weight). Rats were fed a nutritionally adequate liquid diet containing ethanol as 36% of total energy. Controls were fed the same diet in which ethanol was substituted by iso-energetic glucose. At the end of 6 weeks, rats were killed and hearts were fractionated into sarcoplasmic, myofibrillar and stromal protein fractions by differential solubilisation. The total myofibrillar protein content was significantly reduced by chronic ethanol feeding, though the contents of other fractions were relatively unaltered. The fractional and absolute rates of myofibrillar protein synthesis were significantly increased, but the synthesis rates of sarcoplasmic and stromal protein fractions were unaffected by ethanol feeding. This suggests independent regulation of myofibrillar protein content in the ethanol exposed heart. These changes may be responsible for alterations in myocardial function in alcoholic cardiomyopathy.
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Preedy et al. (1989) studied this question.