Abstract
The synthesis of ascorbic acid in rat-liver extracts is impaired during starvation, and more from glucuronolactone and glucuronate than from gulonate and gulonolactone. The formation of xylulose from gulonate and from gulonolactone is greatly enhanced during starvation, whereas it is decreased from glucuronolactone and from glucuronate. The activity of the enzymes of the glucuronic acid pathway during starvation has been determined in rat-liver preparations. Gulonolactone oxidase is decreased, nicotinomide adenine dinucleotide (NAD)-linked gulonate dehydrogenase is enhanced, and uronolactonase, aldonolactonase and nicotinomide adenine dinucleotide phosphate (NADP)-linked hexonate dehydrogenase are unchanged. The impairment of ascorbic acid synthesis from gulonate observed during starvation can be accounted for by the depressed activity of gulonalactone oxidase. The cause of the enhanced formation of xylulose has been located in the sedimentable fraction of liver homogenate. The hypothesis is formulated of an increased utilization of the glucuronic acid pathway during starvation.