Regulation of triacylglycerol hydrolase expression by dietary fatty acids and peroxisomal proliferator-activated receptors
Regulation of triacylglycerol hydrolase expression by dietary fatty acids and peroxisomal proliferator-activated receptors
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DOI：
10.1016/j.bbalip.2003.09.007
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发表时间：
2003-11-30
影响因子：
4.8
通讯作者：
Vance, DE
中科院分区：
文献类型：
--
作者：
Dolinsky, VW;Gilham, D;Vance, DE
三酰甘油水解酶(TGH)是一种催化细胞内储存的三酰甘油(TG)脂解的酶。过氧化物酶体增殖物激活受体(PPAR)调节多种与脂质稳态有关的基因。多不饱和脂肪酸(PUFA)是PPAR的配体，脂肪酸是通过TGH活性产生的，因此我们研究了膳食脂肪和PPAR激动剂是否能调节TGH的表达。在3T3-L1脂肪细胞中，TGH的表达在分化后是前脂肪细胞的10倍。3T3-L1细胞在分化过程中与PPAR-γ激动剂孵育后，TGH的表达较对照细胞增加5倍。没有证据表明PPARGamma直接调节TGH的表达，因为成熟的3T3-L1脂肪细胞与PPARGamma激动剂孵育24小时不影响TGH的表达。饲喂富含脂肪酸的小鼠饲料3周并不影响肝脏TGH的表达，尽管3周的富含脂肪酸和胆固醇的饮食使肝脏TGH的表达增加2倍。两周的氯贝特喂养对野生型或PPARpha缺失小鼠的肝脏TGH表达或微粒体脂解活性没有显著影响，表明PPARpha不调节肝脏TGH的表达。因此，TGH的表达似乎不受肝脏或脂肪细胞中PPAR或脂肪酸的直接调节。(C)2003爱思唯尔B.V.保留所有权利。
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 PPARgamma 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 PPARgamma could not be demonstrated as TGH expression was not affected by a 24-h incubation of mature 3T3-L1 adipocytes with the PPARgamma 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 PPARalpha-null mice, indicating that PPARalpha 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. (C) 2003 Elsevier B.V. All rights reserved.