![]() |
|
|
Department of Biochemistry, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi-110007, India
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.
KEY WORDS: retinyl palmitate vitamin A hypervitaminosis A vitamin A toxicity gluconeogenesis glycolytic enzymes citrate phosphofructokinase pyruvate kinase hexokinase
Manuscript received 27 February 1978.