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Studies of Hepatic Lesions of Experimental Protein-Calorie Malnutrition in Rats and Immediate Effects of Refeeding an Adequate Protein Diet¹

Center for Research in Oral Biology, Departments of Oral Biology and Pathology, Schools of Dentistry and Medicine, University of Washington, Seattle, Washington 98105

In spite of reduced food intake, growing rats (95 to 120 g) fed 0.5% lactalbumin diet ad libitum for periods varying from 6 to 12 weeks developed many of the features found in human protein-calorie malnutrition. The disaggregation of liver polysomes correlated well with the diminished protein synthetic ability of the organ as observed in a cell-free system. Evidence for normal activities of cell sap factors suggested that the defect in protein synthesis in livers of the malnourished rats was due to the quality of the ribosomes. The protein-calorie deficient rat liver exhibited low ribonuclease inhibitor activity as well as increased turnover of ribosomal RNA compared with well-fed controls. Refeeding the animals with adequate diet produced prompt remission of the edema, a shift of ribosomes towards formation of polysomes, diminution of membrane-free monomers and dimers, regeneration of endoplasmic reticulum and a reduction in the fractional daily catabolic rate of ribosomal RNA.

Manuscript received 21 October 1970.