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Papers In Press, published online ahead of print April 21, 2004
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Metabolism Section, Medicine, UCSF, San Francisco, CA 94121
Corresponding Author: grunfld{at}itsa.ucsf.edu
Infection and inflammation, induce the acute-phase response (APR), leading to multiple alterations in lipid and lipoprotein metabolism. Plasma triglyceride levels rise from increased VLDL secretion due to adipose tissue lipolysis, increased de novo hepatic fatty acid synthesis, and suppression of fatty acid oxidation. With more severe infection, VLDL clearance decreases secondary to decreased lipoprotein lipase and apo E in VLDL. In rodents, hypercholesterolemia occurs due to increased hepatic cholesterol synthesis and decreased LDL clearance, conversion of cholesterol to bile acids and secretion of cholesterol into the bile. Marked alterations in proteins important in HDL metabolism lead to decreased reverse cholesterol transport and increased cholesterol delivery to immune cells. Oxidation of LDL and VLDL increase, while HDL becomes a pro-inflammatory molecule. Lipoproteins become enriched in ceramide, glucosylceramide and sphingomyelin, enhancing uptake by macrophages. Thus, many of the changes in lipoproteins are pro-atherogenic. The molecular mechanisms underlying the decrease in many of the proteins during the APR involve coordinate decreases in several nuclear hormone receptors including PPAR, LXR, FXR, and RXR. APR-induced alterations initially protect the host from the harmful effects of bacteria, viruses and parasites. However, if prolonged these changes in the structure and function of lipoproteins will contribute to atherogenesis.
Revised on March 17, 2004
Accepted on April 12, 2004
Effects of infection and inflammation on lipid and lipoprotein metabolism: Mechanisms and consequences to the host
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