Regulation of triacylglycerol hydrolase expression by dietary fatty acids and peroxisomal proliferator-activated receptors |
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Authors: | Vernon W Dolinsky Dean Gilham Grant M Hatch Luis B Agellon Richard Lehner Dennis E Vance |
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Institution: | 1. Department of Biochemistry, University of Alberta, 328 Heritage Medical Research Centre, Edmonton, Alberta, Canada T6G 2S2;2. Department of Cell Biology, University of Alberta, Edmonton, Alberta, Canada T6G 2S2;3. Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada R3E 0T6;4. Department of Pediatrics and the CIHR Group on the Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, Alberta, Canada T6G 2S2 |
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Abstract: | Triacylglycerol hydrolase (TGH) is an enzyme that catalyzes the lipolysis of intracellular stored triacylglycerol (TG). Peroxisomal proliferator-activated receptors (PPAR) regulate a multitude of genes involved in lipid homeostasis. Polyunsaturated fatty acids (PUFA) are PPAR ligands and fatty acids are produced via TGH activity, so we studied whether dietary fats and PPAR agonists could regulate TGH expression. In 3T3-L1 adipocytes, TGH expression was increased 10-fold upon differentiation, compared to pre-adipocytes. 3T3-L1 cells incubated with a PPARγ agonist during the differentiation process resulted in a 5-fold increase in TGH expression compared to control cells. Evidence for direct regulation of TGH expression by PPARγ could not be demonstrated as TGH expression was not affected by a 24-h incubation of mature 3T3-L1 adipocytes with the PPARγ agonist. Feeding mice diets enriched in fatty acids for 3 weeks did not affect hepatic TGH expression, though a 3-week diet enriched in fatty acids and cholesterol increased hepatic TGH expression 2-fold. Two weeks of clofibrate feeding did not significantly affect hepatic TGH expression or microsomal lipolytic activities in wild-type or PPARα-null mice, indicating that PPARα does not regulate hepatic TGH expression. Therefore, TGH expression does not appear to be directly regulated by PPARs or fatty acids in the liver or adipocytes. |
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Keywords: | Triacylglycerol hydrolase Peroxisomal proliferator-activated receptor Adipocyte differentiation aP2 adipocyte lipid binding protein HSL hormone sensitive lipase MUFA monounsaturated fatty acid MUH 4-methylumbelliferyl heptanoate PDI protein disulfide isomerase PPAR peroxisomal proliferator-activated receptor PUFA polyunsaturated fatty acid SFA saturated fatty acids SREBP sterol response element binding protein TG triacylglycerol TGH triacylglycerol hydrolase VLDL very low density lipoprotein |
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