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Cholesterol Consumption Alters Hepatic Sphingomyelin Metabolism in Rats^1,2,

Laboratory of Veterinary Biochemistry ^* Department of Laboratory Animal Science, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands

The hypothesis that cholesterol consumption alters hepatic sphingomyelin homeostasis was tested. Rats were fed a purified diet with or without added cholesterol (1 g/100 g) for up to 21 d. In accordance with previous work, cholesterol consumption significantly increased hepatic, whole plasma and VLDL cholesterol concentrations. Dietary cholesterol also raised the amount of sphingomyelin in the VLDL fraction, which was associated with a decrease in hepatic sphingomyelin concentrations. We suggest that the increase in hepatic VLDL secretion after cholesterol consumption imposed an increase in the demand for sphingomyelin in the liver because this phospholipid is a structural component of VLDL. Determination of the activity of two key enzymes of sphingomyelin homeostasis revealed that cholesterol consumption reduced the activity of acid sphingomyelinase in the liver but did not affect that of serine palmitoyltransferase. These enzyme data indicate that the extra sphingomyelin needed after cholesterol loading results from a decrease in the rate of its catabolism in the liver.

KEY WORDS: • sphingomyelin • dietary cholesterol • liver • lipoproteins • rats

¹ Supported in part by the Netherlands Foundation for Chemical Research (SON) with financial aid from the Netherlands Organization for Scientific Research (NWO). The research by L.B.M.T. was made possible by a fellowship of the Royal Netherlands Academy of Arts and Sciences.

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

³ To whom correspondence should be addressed.

Manuscript received 2 March 1994. Revision accepted 21 March 1995.

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