Tumor necrosis factor, interleukin, and interferon induced changes in lipid metabolism as part of host defense.
As the immune response is activated during infection, multiple changes in lipid metabolism, especially increased production of VLDL, occur. Many of the cytokines that mediate the immune response are able to produce such changes in lipid metabolism in vivo. The induction of hypertriglyceridemia or other changes in lipid metabolism during infection do not directly cause the wasting syndrome. It appears that such changes in lipid metabolism may be beneficial to the host, as lipoproteins inactivate a variety of infectious agents. Cytokine-driven hepatic VLDL production during infection most likely represents a part of the acute phase response. The body is thus able to increase serum lipids during infection, or at least maintain triglyceride-rich lipoproteins despite the anorexia of infection. In this manner, the anti-infective, protective effects of lipoproteins are maintained.
Grunfeld
C
C
Department of Medicine, University of California, San Francisco.
Feingold
K R
KR
D000273:Adipose Tissue / Q000378:metabolism*; D002100:Cachexia / Q000378:metabolism; D002478:Cells, Cultured; D005227:Fatty Acids / Q000378:metabolism; D007109:Immunity; D066298:In Vitro Techniques; D007239:Infections / Q000378:metabolism; D007372:Interferons / Q000494:pharmacology*; D007378:Interleukins / Q000494:pharmacology*; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D005227:Fatty Acids; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; D007372:Interferons