101. Effects of vitamin A deficiency and retinoic acid treatment on expression of a phosphoenolpyruvate carboxykinase-bovine growth hormone gene in transgenic mice
- Author
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Mary M. McGrane, Aiyang Tao, and Dong-Ju Shin
- Subjects
Vitamin ,medicine.medical_specialty ,Receptors, Retinoic Acid ,Biophysics ,Retinoic acid ,Gene Expression ,Retinoic acid receptor beta ,Mice, Transgenic ,Tretinoin ,Biology ,Regulatory Sequences, Nucleic Acid ,Biochemistry ,chemistry.chemical_compound ,Mice ,Internal medicine ,medicine ,Animals ,RNA, Messenger ,Promoter Regions, Genetic ,Molecular Biology ,Vitamin A Deficiency ,Cell Biology ,Retinoid X receptor gamma ,medicine.disease ,Vitamin A deficiency ,Mice, Inbred C57BL ,Retinoic acid receptor ,Endocrinology ,chemistry ,Liver ,Retinoic acid receptor alpha ,Growth Hormone ,Cattle ,Phosphoenolpyruvate Carboxykinase (GTP) ,Phosphoenolpyruvate carboxykinase - Abstract
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)β mRNA levels also change with vitamin A deficiency and supplementation, but not RARα mRNA levels. These results indicate that all-trans RA plays a physiologic role in regulating expression of a gluconeogenic gene in liver.
- Published
- 1995