期刊名称：Journal of Nutritional Science and Vitaminology
印刷版ISSN：0301-4800
电子版ISSN：1881-7742
出版年度：2005
卷号：51
期号：2
页码：124-128
DOI：10.3177/jnsv.51.124
出版社：Center for Academic Publications Japan
摘要：This study investigated the regulation of acetyl-CoA carboxylase (ACC) promoter activity by hormones and nutrients. Genomic clones including promoter I (PI) of the ACC gene were isolated and sequenced. ACC PI fragments (-l, 049/+100 or -220/+21bp) were subcloned into the pGL3-Basic vector that includes luciferase as a reporter gene. The ACC PI/luciferase chimeric plasmids were transfected into primary rat hepatocytes using lipofectin. Insulin treatment increased the activity of -1, 049/+100 and -220/+21 ACC PI by 3.0- and 3.5-fold, respectively, compared to the control. The activity of both con-structs was also increased by dexamethasone (Dex) and triiodothyronine (T3), with the greatest effects seen with all three hormones present. With -1, 049/+100 or -220/+21 ACC PI, the addition of glucose increased luciferase activity compared to glucose-free con-trol ( p <0.05). On the other hand, polyunsaturated fatty acids (PUFA) reduced the activity of the -1, 0491+100 ACC PI construct, with eicosapentaenoic acid and docosahexaenoic acid showing the greatest effect (about 70% of the control). However, the addition of PUFA to the culture media did not affect the activity of -220/+21 ACC PI. Therefore, insulin, Dex, T3, glucose, and PUFA regulate ACC gene expression, at least in part, through the PI promoter.
