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Papers In Press, published online ahead of print March 16, 2005
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Division of Biopharmaceutics, LACDR, Gorlaeus Laboratories, Leiden 2333CC
Corresponding Author: r.out{at}lacdr.leidenuniv.nl
The function of scavenger receptor class B type I (SR-BI) in mediating the selective uptake of HDL cholesterol esters is well established. In SR-BI deficient mice we recently observed a delayed postprandial triglyceride response (Out et al., J.Biol.Chem, 279 (2004)18401-18406) suggesting an additional role for SR-BI in facilitating chylomicron metabolism. In the present investigation, we assessed the effect of adenovirus-mediated hepatic overexpression of SR-BI (Ad.SR-BI) in C57BL/6J mice on serum lipids and chylomicron metabolism. Infection of 5x108 pfu per mouse of Ad.SR-BI significantly decreases serum cholesterol (>90%), phospholipids (>90%), and triglyceride levels (50%), accompanied by a 41.4% reduction (p<0.01) in apoB100 levels. The relevance of SR-BI overexpression for in vivo chylomicron (remnant) metabolism was evaluated by studying the effect on an intra-gastric fat load-induced postprandial triglyceride response. The postprandial triglyceride response is 2-fold lower in mice treated with Ad.SR-BI compared to control mice (area-under-the curve 31.4 ± 2.4 versus 17.7 ± 3.2; P<0.05). Hepatic expression levels of genes known to be involved in serum cholesterol and triglyceride clearance were tested by real-time PCR and it appears that the mRNA expression levels of the LDLr, LRP1, ABCA1, HMG-CoA reductase, ABCG1, ABCG5, ABCG8, CYP7A1, CYP27, BSEP, hepatic lipase, and lipoprotein lipase are unchanged and thus could not account for the decreased plasma triglyceride levels and the change in postprandial response. We conclude that overexpression of SR-BI accelerates chylomicron metabolism possibly by mediating the initial capture of chylomicron remnants by the liver whereby the subsequent internalization can be exerted by additional receptor systems like the LDL receptor and LRP1.
Revised on February 23, 2005
Accepted on March 8, 2005
Adenovirus-mediated hepatic overexpression of scavenger receptor BI accelerates chylomicron metabolism in C57BL/6J mice
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