Retinoic acid, bound to its nuclear receptor, enhances the expression of the gene for phosphoenolpyruvate carboxykinase.
Over 30 years ago, whole-animal studies conclusively showed that liver glycogen depletion in vitamin A deficiency was caused by depressed gluconeogenesis. The techniques of modern cell and molecular biology have now been utilized to demonstrate the probable molecular pathogenesis of this defect associated with vitamin A deficiency. Retinoic acid, bound to its nuclear receptor, stimulates transcription of the gene for phosphoenolpyruvate carboxykinase (PEPCK), the rate-limiting enzyme in gluconeogenesis, by binding to a short element of the promoter region of the PEPCK gene.
D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism*; D002467:Cell Nucleus / Q000378:metabolism; D015971:Gene Expression Regulation, Enzymologic; D010729:Phosphoenolpyruvate Carboxykinase (GTP) / Q000235:genetics*; D011401:Promoter Regions, Genetic; D018168:Receptors, Retinoic Acid; D014158:Transcription, Genetic; D014212:Tretinoin / Q000378:metabolism*
D002352:Carrier Proteins; D018168:Receptors, Retinoic Acid; D014212:Tretinoin; D010729:Phosphoenolpyruvate Carboxykinase (GTP)