Submitted on August 9, 2005
Revised on October 25, 2005
Accepted on October 25, 2005
Absorption and lipoprotein transport of sphingomyelin
Åke Nilsson and Rui-Dong Duan
Institution of Medicine, Lund University, Lund S-221 84
Corresponding Author: ake.nilsson{at}med.lu.se
Dietary sphingomyelin (SM) is hydrolyzed by intestinal alkaline sphingomyelinase and neutral ceramidase to sphingosine, which is absorbed and converted to palmitic acid and acylated into chylomicron triglycerides. SM digestion is slow and is affected by luminal factors such as bile salt, cholesterol, and other lipids. In the gut SM and its metabolites may influence triglyceride hydrolysis, cholesterol absorption, lipoprotein formation and mucosal growth. SM accounts for about 20 % of the phospholipids in human plasma lipoproteins of which two thirds are in LDL and VLDL. It is secreted in chylomicrons and VLDL and transferred into HDL via the ABCA1 transporter. Plasma SM increases after large lipid loads, during suckling, and in type II hypercholesterolemia, cholesterol fed animals, and apoE deficient mice. SM is thus an important amphiphilic component when plasma lipoprotein pools expand in response to large lipid loads or metabolic abnormalities. It inhibits lipoprotein lipase and LCAT, and the interaction of lipoproteins with receptors, and counteracts LDL oxidation. Turnover of plasma SM is larger than can be accounted for by the turnover of LDL and HDL particles. Some SM must be degraded via receptor mediated catabolism of chylomicron- and VLDL remnants and by SR-BI receptor mediated transfer into cells.
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