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本文引用的文献

1
Cloning and characterization of the 5' end and promoter region of the chicken acetyl-CoA carboxylase gene.鸡乙酰辅酶A羧化酶基因5'端及启动子区域的克隆与特性分析
Biochem J. 1996 Mar 1;314 ( Pt 2)(Pt 2):613-9. doi: 10.1042/bj3140613.
2
Regulation of the long-chain carnitine acyltransferases.长链肉碱酰基转移酶的调节
FASEB J. 1993 Aug;7(11):1039-44. doi: 10.1096/fasebj.7.11.8370473.
3
Brain acetyl-CoA carboxylase: isozymic identification and studies of its regulation during development and altered nutrition.脑乙酰辅酶A羧化酶:同工酶鉴定及其在发育过程和营养改变时的调节研究
Biochem Biophys Res Commun. 1993 Apr 30;192(2):820-5. doi: 10.1006/bbrc.1993.1488.
4
Unique structural features and differential phosphorylation of the 280-kDa component (isozyme) of rat liver acetyl-CoA carboxylase.大鼠肝脏乙酰辅酶A羧化酶280-kDa组分(同工酶)的独特结构特征和差异磷酸化作用
J Biol Chem. 1994 May 20;269(20):14438-45.
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Physiological and molecular mechanisms involved in nutritional regulation of fatty acid synthesis.脂肪酸合成的营养调控所涉及的生理和分子机制。
Physiol Rev. 1995 Jan;75(1):47-76. doi: 10.1152/physrev.1995.75.1.47.
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Essentiality of dietary carbohydrate for maintenance of liver lipogenesis in the chick.雏鸡维持肝脏脂肪生成所需的膳食碳水化合物
J Nutr. 1980 Aug;110(8):1533-42. doi: 10.1093/jn/110.8.1533.
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A technique for radiolabeling DNA restriction endonuclease fragments to high specific activity.一种将DNA限制性内切酶片段放射性标记至高比活度的技术。
Anal Biochem. 1983 Jul 1;132(1):6-13. doi: 10.1016/0003-2697(83)90418-9.
8
Two promoters of different strengths control the transcription of the mouse alpha-amylase gene Amy-1a in the parotid gland and the liver.两种不同强度的启动子控制着小鼠腮腺和肝脏中α-淀粉酶基因Amy-1a的转录。
Cell. 1983 Jun;33(2):501-8. doi: 10.1016/0092-8674(83)90431-2.
9
Coordinate suppression of liver acetyl-CoA carboxylase and fatty acid synthetase by polyunsaturated fat.多不饱和脂肪对肝脏乙酰辅酶A羧化酶和脂肪酸合成酶的协同抑制作用
J Nutr. 1981 Jan;111(1):146-53. doi: 10.1093/jn/111.1.146.
10
Purification of rat liver acetyl coenzyme A carboxylase and immunochemical studies on its synthesis and degradation.大鼠肝脏乙酰辅酶A羧化酶的纯化及其合成与降解的免疫化学研究。
Eur J Biochem. 1970 Sep;16(1):161-73. doi: 10.1111/j.1432-1033.1970.tb01068.x.

营养状况的改变通过转录机制调节禽类肝脏中乙酰辅酶A羧化酶的表达。

Alterations in nutritional status regulate acetyl-CoA carboxylase expression in avian liver by a transcriptional mechanism.

作者信息

Hillgartner F B, Charron T, Chesnut K A

机构信息

Department of Biochemistry, School of Medicine, West Virginia University, Morgantown 26506, USA.

出版信息

Biochem J. 1996 Oct 1;319 ( Pt 1)(Pt 1):263-8. doi: 10.1042/bj3190263.

DOI:10.1042/bj3190263
PMID:8870677
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1217763/
Abstract

Feeding previously starved chicks with a high-carbohydrate, low-fat diet stimulates a 9-fold increase in both the rate of synthesis of acetyl-CoA carboxylase (ACC) and the abundance of its mRNA in liver. To define the steps involved in mediating diet-induced changes in the abundance of ACC mRNA, transcriptional activity was measured with the nuclear run-on assay and multiple DNA probes specific to the ACC gene. ACC transcription was low in livers of starved chicks; feeding them with a high-carbohydrate, low-fat diet induced ACC transcription, increasing it 11-fold. An increase in transcription was detectable at 1 h, was maximal at 5 h and remained high for 26 h. Feeding previously starved chicks with a low-carbohydrate, high-fat diet stimulated a smaller increase (4-fold) in the abundance of ACC mRNA and the transcription of ACC than feeding with a high-carbohydrate, low-fat diet. The half-life of ACC mRNA in liver, as estimated from the kinetics of accumulation and decay of ACC mRNA during high-carbohydrate feeding and starvation, was not changed significantly by dietary manipulation. ACC mRNA was expressed at low levels in heart, pectoral muscle, kidney and brain. The abundance of ACC mRNA in these tissues was not affected by nutritional manipulation. These results demonstrate that nutritional control of the abundance of ACC mRNA in the chicken is liver-specific and is mediated primarily by changes in the rate of transcription of the ACC gene.

摘要

用高碳水化合物、低脂肪饮食喂养先前饥饿的雏鸡,会刺激肝脏中乙酰辅酶A羧化酶(ACC)的合成速率及其mRNA丰度增加9倍。为了确定介导饮食诱导的ACC mRNA丰度变化所涉及的步骤,使用核转录分析和针对ACC基因的多个DNA探针测量转录活性。在饥饿雏鸡的肝脏中,ACC转录水平较低;用高碳水化合物、低脂肪饮食喂养它们会诱导ACC转录,使其增加11倍。在1小时时可检测到转录增加,在5小时时达到最大值,并在26小时内保持高水平。用低碳水化合物、高脂肪饮食喂养先前饥饿的雏鸡,与用高碳水化合物、低脂肪饮食喂养相比,刺激ACC mRNA丰度和ACC转录的增加幅度较小(4倍)。根据高碳水化合物喂养和饥饿期间ACC mRNA积累和衰减的动力学估计,肝脏中ACC mRNA的半衰期不受饮食操作的显著影响。ACC mRNA在心脏、胸肌、肾脏和大脑中低水平表达。这些组织中ACC mRNA的丰度不受营养操作的影响。这些结果表明,鸡中ACC mRNA丰度的营养控制是肝脏特异性的,并且主要由ACC基因转录速率的变化介导。