Shin D J, Tao A, McGrane M M
Department of Nutritional Sciences, University of Connecticut, Storrs 06269, USA.
Biochem Biophys Res Commun. 1995 Aug 15;213(2):706-14. doi: 10.1006/bbrc.1995.2188.
Vitamin A regulation of specific promoter domains of the phosphoenolpyruvate carboxykinase (PEPCK) gene was tested in a PEPCK/bovine growth hormone (bGH) transgenic mouse model. Vitamin A deficiency causes a significant decrease in hepatic bGH mRNA when expression is driven by either a 533-base-pair (bp) PEPCK promoter fragment (from position -460 to +73) or a 428-bp PEPCK promoter fragment (from position -355 to +73). Treatment of vitamin A deficient transgenic mice with all-trans retinoic acid (RA) increases bGH mRNA levels above those measured with the deficiency. Hepatic retinoic acid receptor (RAR)beta mRNA levels also change with vitamin A deficiency and supplementation, but not RAR alpha mRNA levels. These results indicate that all-trans RA plays a physiologic role in regulating expression of a gluconeogenic gene in liver.
在磷酸烯醇式丙酮酸羧激酶（PEPCK）/牛生长激素（bGH）转基因小鼠模型中，对维生素A对PEPCK基因特定启动子结构域的调控作用进行了测试。当由一个533碱基对（bp）的PEPCK启动子片段（从-460位至+73位）或一个428 bp的PEPCK启动子片段（从-355位至+73位）驱动表达时，维生素A缺乏会导致肝脏bGH mRNA显著下降。用全反式视黄酸（RA）处理维生素A缺乏的转基因小鼠，可使bGH mRNA水平升高至高于缺乏状态下测得的水平。肝脏视黄酸受体（RAR）β mRNA水平也会随维生素A缺乏和补充而变化，但RARα mRNA水平则不然。这些结果表明，全反式RA在调节肝脏中糖异生基因的表达方面发挥着生理作用。
