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Role of Triacylglycerol Hydrolase and Apolipoprotein E in Hepatic Lipid Droplet Metabolism
Author(s) -
Wang Huajin,
Lehner Richard
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.807.9
Subject(s) - very low density lipoprotein , lipid droplet , apolipoprotein e , apolipoprotein b , secretion , lipid metabolism , lipoprotein , microbiology and biotechnology , chemistry , biology , biochemistry , medicine , cholesterol , disease
The objective of the study was to address the roles of triacylglycerol hydrolase (TGH) and apolipoprotein E (apoE) in the mobilization of hepatic triacylglycerol (TG) stores for very‐low density lipoprotein (VLDL) assembly. TGH and apoE associate with the same pool of hepatic luminal lipid droplets (LLD) and potentially interact with each other. Lack of TGH or apoE expression alters hepatic TG storage in both the cytosolic lipid droplets (CLD) and in the luminal lipid droplets (LLD), suggesting a crosstalk between the two lipid storage pools. Metabolic labeling studies revealed that ectopic expression of TGH channels the cytosolic rather than the luminal pool of TG for VLDL secretion. Accordingly, it is also observed by confocal imaging that the absence of TGH or apoE alters CLD morphology and distribution in hepatocytes. Apo E deficiency results in redistribution of LLD‐associated proteins, suggesting a role for apoE in altering LLD protein composition. ApoE is also found to translocate to CLD in TGH deficient hepatocytes, indicating correlated roles of TGH and apoE. It is concluded that TGH, in concert with apoE, channels mainly CLD‐TG for VLDL secretion and plays a critical role in regulating lipid droplet formation, morphology and protein composition. Supported by the a grant from the Canadian Institutes of Health Research