Journal of Nutrition and Health

The Korean Nutrition Society (한국영양학회)
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Hormonal Regulation of Acetyl-CoA Carboxylase Promoter I Activity in Rat Primary Hepatocytes

흰쥐의 간세포에서 호르몬에 의한 Acetyl-CoA Carboxylase Promoter I Activity 조절에 대한 연구

  • 이막순 (창원대학교 식품영양학과) ;
  • 양정례 (창원대학교 생활과학연구소) ;
  • 김윤정 (창원대학교 생활과학연구소) ;
  • 김영화 (창원대학교 생활과학연구소) ;
  • 김양하 (창원대학교 식품영양학과)
  • Published : 2002.03.01
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Abstract

Acetyl-CoA carboxylase (ACC) is the enzyme that controls no devo fatty acid biogynthesis, and this enzyme catalyzes the carboxylation pathway of acetyl-CoA to malonyl-CoA. Acetyl-CoA carboxylase gene expression was regulated by nutritional and hormonal status. The present study was performed to identify the regulation mechanism of ACC gene promoter I. The fragments of ACC promoter I -1.2-kb region wert recombined to pGL3-Basic vector with luciferase as a reporter gene. The primary hepatocytes from the rat were used to investigate the hormonal regulation of ACC promoter I activity. ACC PI (-1.2)/Luc plasmid was trtransferred into primary hepatocytes using lipofectin. Activity of luciferase was increased two-fold by 10-9M, three-fold by 10-8M, 10-6M, 3.5-fold by 10-6M, and 4.5-fold by 10-7M insulin treatment, respectively. In the presence of dexamethasone (1 $\mu$M), the effects of insulin increased about 1.5-fold, showing the additional effects of dexamethasone. Moreover, the activity of luciferase increased with insulin+dexamethasone, insulin+T3, dexamethasone+T3, and dexamethasone+insulin+T3 treatment approximately 6-, 4-, 6.5-, and 10-fold, respectively. Therefore it can be postulated that 1) these hormones coordinately regulate acetyl-CoA caroxylase gene expression via regulation of promoter activity, 2) the -1.2-kb region of ACC promoter I may have the response element sequences for insulin, dexamethasone, and T3.

Keywords

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