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Sci. STKE, 17 April 2007
Vol. 2007, Issue 382, p. tw136
[DOI: 10.1126/stke.3822007tw136]


Medicine Making LIGHT of Lipid Metabolism

Stephen Simpson

Science, AAAS, Cambridge CB2 1LQ, UK

Atherosclerosis results from a combination of lipid dysregulation and inflammation-mediated pathology of the vasculature. Lo et al. show that increased expression of related members of the tumor necrosis factor family of inflammatory cytokines, LIGHT and lymphotoxin (LT), on T cells can elevate circulating blood cholesterol and triglycerides in mice. This effect appeared to be mediated via lymphotoxin beta receptor (LTbetaR) signaling in hepatocytes, leading to a drop in the activity of hepatic lipase, an enzyme central to lipid metabolism. The normally high lipid levels found in mice that lack the low-density lipoprotein receptor gene were reduced when LTbetaR signaling was inhibited. These results raise questions about how the immune system detects and subsequently exacerbates dyslipidemia and whether this process makes any direct contribution to atherosclerosis in humans.

J. C. Lo, Y. Wang, A. V. Tumanov, M. Bamji, Z. Yao, C. A. Reardon, G. S. Getz, Y.-X. Fu, Lymphotoxin beta receptor-dependent control of lipid homeostasis. Science 316, 285-288 (2007). [Abstract] [Full Text]

G. K. Hansson, LIGHT hits the liver. Science 316, 206-207 (2007). [Summary] [Full Text]

Citation: S. Simpson, Making LIGHT of Lipid Metabolism. Sci. STKE 2007, tw136 (2007).

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