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.