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Puromycin aminonucleoside (PA) nephrosis in the rat was accompanied by hyperlipæmia, with raised serum concentrations of triglycerides, total cholesterol, triglyceride/total cholesterol ratio, phospholipids (mainly lecithin), and alpha and beta lipoprotein lipids. Marked changes occurred in liver metabolism, with Increases in liver weight, total protein, microsomal protein and microsomal drug-metabolizing enzymes. PA-nephrotic hyperlipæmia offered an excellent model tor testing antilipæmic drugs. Ethyl chlorophenoxyisobutyrate (“Atromid-S”) and sodium betabenzalbutyrate (“Kata-Lipid”) effectively controlled the hyperlipæmia. Chlorophenoxyisobutyrate caused further hepatomegaly and induction of drug-metabolizing enzymes, but betabenzalbutyrate did not, adding indirect support to the hypothesis that these chemically related drugs may have different modes of action. Nephrotic hyperlipæmia in man commonly remains untreated, although accelerated atherosclerosis and thromboses frequently occur. The application of new methods of controlling nephrotic hyperlipæmia in man is urgently required.
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Edwards et al. (1970) studied this question.
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