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3T3-L1脂肪细胞中细胞溶质磷酸烯醇式丙酮酸羧激酶的表达与调控

Expression and regulation of cytosolic phosphoenolpyruvate carboxykinase in 3T3-L1 adipocytes.

作者信息

Beale E G, Tishler E J

机构信息

Department of Cell Biology and Anatomy, Texas Tech University Health Sciences Center, School of Medicine, Lubbock 79430.

出版信息

Biochem Biophys Res Commun. 1992 Dec 15;189(2):925-30. doi: 10.1016/0006-291x(92)92292-6.

Abstract

Animal studies have shown that the gene encoding cytosolic phosphoenolpyruvate carboxykinase (PEPCK) is controlled by unique mechanisms in fat. For example, a unique cis-acting DNA sequence located 1-2 kilobase pairs upstream of the promoter is required for PEPCK gene expression in adipocytes but not in other cell types. Moreover, glucocorticoids repress PEPCK gene transcription in fat whereas these steroids induce the same gene in liver and kidney. An in vitro system of cultured adipocytes would greatly facilitate studies of PEPCK gene regulation in fat cells. In this study, we report that cultured 3T3-L1 cells activate the PEPCK gene upon differentiation from fibroblasts to adipocytes. In addition, we report that cAMP induces and insulin and dexamethasone repress PEPCK mRNA in 3T3-L1 adipocytes. Thus these cells may provide a useful model system for future studies.

摘要

动物研究表明,编码胞质磷酸烯醇式丙酮酸羧激酶(PEPCK)的基因在脂肪组织中受独特机制调控。例如,启动子上游1 - 2千碱基对处的一个独特顺式作用DNA序列是脂肪细胞中PEPCK基因表达所必需的,但在其他细胞类型中并非如此。此外,糖皮质激素会抑制脂肪组织中PEPCK基因的转录,而这些类固醇激素在肝脏和肾脏中会诱导该基因表达。培养的脂肪细胞体外系统将极大地促进对脂肪细胞中PEPCK基因调控的研究。在本研究中,我们报告培养的3T3 - L1细胞在从成纤维细胞分化为脂肪细胞时会激活PEPCK基因。此外,我们报告cAMP可诱导3T3 - L1脂肪细胞中的PEPCK mRNA表达,而胰岛素和地塞米松则会抑制其表达。因此,这些细胞可能为未来的研究提供一个有用的模型系统。

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