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Papers In Press, published online ahead of print October 14, 2005
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The Wallenberg Laboratory, University of Göteborg, Göteborg SE-413 45
Corresponding Author: Sven-Olof.Olofsson{at}medkem.gu.se
Epigallocatechin gallate (EGCG) increases the formation of cytosolic lipid droplets by a mechanism that is independent of the rate of triglyceride biosynthesis, and involves an enhanced fusion between lipid droplets, a process that is crucial for their growth in size. EGCG treatment reduced the secretion of both triglycerides and apoB-100 VLDLs but not of transferrin, albumin or total proteins, indicating that EGCG diverts triglycerides from VLDL assembly to storage in the cytosol. This is further supported by the observed increase in both intracellular degradation of apoB-100 and ubiquitination of the protein (indicative of increased proteasomal degradation) in EGCG-treated cells. EGCG did not interfere with the microsomal triglyceride transfer protein, and the effect of EGCG on the secretion of VLDLs was found to be independent of the LDL receptor. Thus, our results indicate that EGCG promotes the accumulation of triglycerides in cytosolic lipid droplets, thereby diverting lipids from the assembly of VLDL to storage in the cytosol. Our results also indicate that the accumulation of lipids in the cytosol is not always associated with increased secretion of VLDL.
Revised on October 13, 2005
Accepted on October 14, 2005
Epigallocatechin gallate promotes the formation of cytosolic lipid droplets and causes a subsequent reduction in the assembly and secretion of VLDL-containing apoB-100
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