Early effects of vitamin A toxicity on hepatic glycolysis in rat.
Vitamin A toxicity, caused by oral administration of 30,000 IU of vitamin A (retinyl palmitate) to young rats (70 to 90 g) once daily for 2 days, increased the levels of lipids, glycogen, and citrate in the liver. Furthermore, hypervitaminosis A decreased the activities of two key hepatic glycolytic enzymes, phosphofructokinase, and pyruvate kinase, without affecting those of hexokinase and glucokinase. It is suggested, therefore, that in addition to the increased activities of key gluconeogenic enzymes, reported earlier, a marked decrease in the activities of phosphofructokinase and pyruvate kinase and elevated level of citrate in the liver could account for the enhanced gluconeogenesis in hypervitaminosis A.
D000818:Animals; D002951:Citrates / Q000494:pharmacology; D005943:Gluconeogenesis / Q000187:drug effects; D006019:Glycolysis / Q000187:drug effects*; D006593:Hexokinase / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D010732:Phosphofructokinase-1 / Q000378:metabolism; D011770:Pyruvate Kinase / Q000378:metabolism; D051381:Rats; D014801:Vitamin A / Q000633:toxicity*
D002951:Citrates; D014801:Vitamin A; D006593:Hexokinase; D010732:Phosphofructokinase-1; D011770:Pyruvate Kinase