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Hormones and nutrients regulate acetyl-CoA carboxylase promoter I in rat primary hepatocytes
- Hormones and nutrients regulate acetyl-CoA carboxylase promoter I in rat primary hepatocytes
- Kim Y.-J.; Lee M.-S.; Lee H.-J.; Wu Y.; Freake H.C.; Chun H.-S.; Kim Y.
- Ewha Authors
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- Journal of Nutritional Science and Vitaminology
- Journal of Nutritional Science and Vitaminology vol. 51, no. 2, pp. 124 - 128
- SCIE; SCOPUS
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- 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 (-1,049/+100 or -220/+21 bp) 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 constructs 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 control (p<0.05). On the other hand, polyunsaturated fatty acids (PUFA) reduced the activity of the -1,049/+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, T 3, glucose, and PUFA regulate ACC gene expression, at least in part, through the PI promoter.
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