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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2003.3
- 수록면
- 61 - 65 (5page)
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초록· 키워드
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This study was investigated to identify the regulatory mechanism of ACC gene expression by hormones, nutrition. The fragment of ACC promoter I (PI) -220 bp region was recombined to pGL3-Basic vector with luciferase as a reporter gene. The primary hepatocyte from the rat was used to investigate the regulation of ACC PI activity. ACC PI (-220 bp)/luciferase chimeric plasmid was transfected into primary rat hepatocyte by using lipofectin. ACC PI activity was shown by measuring luciferase activity. The addition of insulin, dexamethasone,, triiodothyronine to the culture medium increased the activity of ACC PI by 2.5-, 2.3-, 1.8-fold, respectively. In the presence of 1 μM dexamethasone, the effects of insulin was amplified about 1.2-fold showing the additional effects of dexamethasone. Moreover the activity of luciferase was increased by insulin, dexamethasone,, triiodothyronine treatment approximately 4-fold. These results indicated that insulin, dexamethasone, thyroid hormone coordinately regulate ACC gene expression via regulation of promoter I activity. On the -220 to +21 region of ACC PI, the addition of the glucose to the culture medium increased the activity of ACC PI. With 25 mM glucose, luciferase activity increased by 7-fold. On the other hand, on the -220 bp region, ACC PI activity was not changed by polyunsaturated fatty acids. Therefore, it can be postulated that there are response elements for insulin, triiodothyronine, dexamethasone,, glucose, but not PUFAs on the -220 bp region of ACC PI.
목차
Abstract
INTRODUCTION
MATERIALS AND METHODS
RESULTS AND DISCUSSION
ACKNOWLEDGEMENT
REFERENCES
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UCI(KEPA) : I410-ECN-0101-2009-511-018079006