Biosynthesis of Ascorbic Acid and Prevention of Glycogen Depletion in Liver and Muscle

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Abstract
Biosynthesis of ascorbic acid in rats is stimulated by sodium acetoacetate up to a certain concentration (300 mg/kg). Acetoacetate in higher concentration (600 mg/kg), depresses such biosynthesis in rats. Rabbits fail to synthesize ascorbic acid after acetoacetate injection. Sodium beta-hydroxybutyrate, another member of the acetone bodies, has no stimulating influence on the biosynthesis of ascorbic acid either in rats or in rabbits. A relationship between plasma ascorbic acid level and glycogen storage in liver and muscle of rats was observed. The animals (rats), which show lowered concentration of ascorbic acid after repeated injections of acetoacetate (500 mg/kg) have less glycogen in liver and muscle. Glycogen storage in liver and muscle is normal in those animals which show normal blood ascorbic acid level after acetoacetate injections in lower concentration (200 mg/kg). The failure of acetoacetate in depleting liver and muscle glycogen of rats when injected in lower concentration (200 mg/kg) was attributed to ascorbic acid biosynthesis, which was stimulated by acetoacetate at such concentration.