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首页> 外文期刊>Pediatric surgery international >Regulation of FAT/CD36 mRNA gene expression by long chain fatty acids in the differentiated 3T3-L1 cells.
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Regulation of FAT/CD36 mRNA gene expression by long chain fatty acids in the differentiated 3T3-L1 cells.

机译:长链脂肪酸对分化的3T3-L1细胞中FAT / CD36 mRNA基因表达的调节。

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Defects in fatty acid translocase (FAT/CD36) have been identified as a major factor in insulin resistance and defective fatty acid and glucose metabolism. Therefore, understanding of the regulation of FAT/CD36 expression and function is important for a potential therapeutic target for type II diabetes. We differentiated 3T3-L1 preadipocytes into matured adipocytes and examined the roles of insulin and long chain fatty acids on FAT/CD36 expression and function. Our results indicate that FAT/CD36 mRNA expression was not detected at preadipocyte but was significantly increased at matured adipocyte. In fully differentiated 3T3-L1 adipocytes, insulin significantly increased FAT/CD36 mRNA and protein expression in a dose dependent manner. The free fatty acid stearic acid reduced FAT/CD36 mRNA expression while the non-metabolizable free fatty acid alpha-bromopalmitate (2-BP) significantly increased FAT/CD36 mRNA and protein expression. Isoproterenol, in contrast, dose-dependently reduced FAT/CD36 mRNA expression and increased free fatty acid release. Mechanism analysis indicated that the effect of insulin and 2-BP on the FAT/CD36 mRNA gene expression may be mediated through activation of PPAR-gamma, suggesting that FAT/CD36 may have important implications in the pathophysiology of defective fatty acid metabolism.
机译:脂肪酸转位酶(FAT / CD36)的缺陷已被确定为胰岛素抵抗,脂肪酸和葡萄糖代谢不良的主要因素。因此,了解FAT / CD36表达和功能的调节对于II型糖尿病的潜在治疗靶点很重要。我们将3T3-L1前脂肪细胞分化为成熟的脂肪细胞,并检查了胰岛素和长链脂肪酸对FAT / CD36表达和功能的作用。我们的结果表明,在脂肪前细胞中未检测到FAT / CD36 mRNA表达,但在成熟的脂肪细胞中FAT / CD36 mRNA表达显着增加。在完全分化的3T3-L1脂肪细胞中,胰岛素以剂量依赖性方式显着增加FAT / CD36 mRNA和蛋白质表达。游离脂肪酸硬脂酸降低FAT / CD36 mRNA表达,而不可代谢的游离脂肪酸α-溴棕榈酸酯(2-BP)显着增加FAT / CD36 mRNA和蛋白表达。相反,异丙肾上腺素剂量依赖性地降低FAT / CD36 mRNA表达并增加游离脂肪酸释放。机理分析表明,胰岛素和2-BP对FAT / CD36 mRNA基因表达的影响可能是通过激活PPAR-γ介导的,提示FAT / CD36可能在脂肪酸代谢缺陷的病理生理中具有重要意义。

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