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A more recent version of this article appeared on July 1, 2003

Papers In Press, published online ahead of print April 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300123-JLR200
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Submitted on March 21, 2003
Revised on April 9, 2003
Accepted on April 16, 2003

Inhibition of carnitine palmitoyltransferase in the rat small intestine reduces export of triacylglycerol into the lymph

LaTonya Washington, Geoge A. Cook, and Charles M. Mansbach II

Medicine/Gastroenterology, The University of Tennessee, Memphis, TN 38118

Corresponding Author: CMANSBACH{at}UTMEM.EDU

Following digestion of dietary triacylglycerol, intestinal epithelial cells absorb fatty acids and monoacylglycerols which are re-synthesized to triacylglycerol by enzymes located on the endoplasmic reticulum. An in vitro study in rat liver (Abu-Hashema et al. J. Biol. Chem.:274: 35577-35582, 1999) showed that there is a carnitine dependent ER lumenal synthesis of TAG presumably contributing to hepatic lipoprotein synthesis. We wished to test the hypothesis that a similar pathway was present in the rat intestine in vivo leading to chylomicron export by utilizing etomoxir, which, as its CoA derivative, inhibits carnitine acyl transferase activity. Infusion of etomoxir into the lumen of the small intestine inhibited carnitine acyltransferase activity in endoplasmic reticulum subsequently isolated from enterocytes (69 %). Etomoxir did not affect either the uptake of intraduodenally infused 3H-glyceryltrioleate by the intestinal mucosa or the production of mucosal 3H-triacylglycerol, excluding the possibility that etomoxir interfered with triacylglycerol absorption or synthesis. Etomoxir did not inhibit protein synthesis, glucose, cholesterol or palmitate absorption or metabolism or ATP concentrations. Etomoxir substantially (74 %) diminished lymph triacylglycerol output from intralumenally infused glyceryltrioleate. In conclusion, these data strongly support the hypothesis that an endoplasmic reticulum carnitine palmitoyltransferase system exists and is necessary for processing dietary triacylglycerol into chylomicrons. The significant reduction in lymphatic output of chylomicron triacylglycerol on etomoxir treatment suggests that the major source of chylomicron triacylglycerol is a diacylglyceroltransferase on the lumenal surface of the endoplasmic reticulum.


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