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Ribose 5-phosphate occupies an important position as an intermediate in the oxidative or pentose phosphate pathway of glucose metabolism. In both plant and animal tissues ribose 5-phosphate forms fructose 6-phosphate ( 1 ) which may be readily converted to glucose. Recently Agranoff and Brady(2) have isolated an enzyme from mammalian liver capable of phosphorylating D-ribose to form ribose 5-phosphate, thus permitting ribose to enter into this pathway. The conversion of ribose to glucose has been demonstrated by Katz et d ( 3 ) who found that ribose l-C14 incubated with rat liver slices yielded glucose labeled in a pattern which agreed with predictions from known reactions. Intravenous infusion of known glycogenic sugars such as D-galactose (4) and D-fructose (5,6) have been shown to cause an increase in blood glucose levels in normal man. Occurrence of increases in blood glucose levels after infusion of the pentoses D-xylose and L-arabinose has been reported from this laboratory although no effect was observed after D-lyxose and Darabinose administration ( 7 ) .Bruck and Rapoport (8) have reported that D-galactose * Present address: Duke University School of Medicine, Durham, N. C.infusions cause a lowering of blood glucose levels in galactosemic individuals. Except for a single observation that infusion of Dfructose may have a glucose lowering effect (9) no sugars have been observed to cause decreases in blood glucose levels following infusion into normal man. This paper reports that following infusion of D-ribose into normal man, decreases in blood glucose levels occur despite the fact that this sugar is susceptible to conversion to glucose via known metabolic pathways.Methods. The D-ribose used was obtained from the Pfanstiehl Co., Waukegan, Ill. By the criteria of optical rotation and paper chromatography, the sugar was authentic Dribose. Fifteen infusions of D-ribose were performed in 5 fasting normal males, (ages 18-21 yrs.) 3 diabetics (ages 23, 31 and 53 yrs.) whose last insulin dose (NPH + crystalline) was given 24 hours prior to study and one 48 yr. old subject with liver disease proved by liver biopsy. D-ribose was autoclaved as a 7.576 solution and found sterile and pyrogen-free prior to use. In 13 studies, 10 to 20 g of D-ribose were infused intravenously over 10-25 minutes. Blood specimens were obtained from an indwelling plasat GEORGETOWN UNIV MED CTR on July 20, 2015 ebm.sagepub.com Downloaded from

In 1931 Wierzuchowski (1) showed an influence of insulin on galactose tolerance of dogs. More recently, Levine, Goldstein, Huddlestun, Klein, and Henry (2, 3) demonstrated that insulin lowers the blood levels of D-galactose, D-xylose, and L-arabinose but not of D-arabinose or D-mannose, following their infusion into the eviscerated nephrectomized dog. The volume of distribution of the responsive sugars was increased from 45 to 70 per cent of body weight as a result of insulin administration. It was suggested that the insulin response represented a facilitation of transport of the sugar across the cell membrane into intracellular fluid. In all the responsive sugars the stereochemical structure of carbon atoms 1 to 3 was like that of D-glucose, and these authors suggested that these structural characteristics determined the insulin responsiveness of a sugar.Confirmatory evidence has appeared that insulin affects transport of D-galactose, D-xylose and L-arabinose across the cell membrane in the rat diaphragm (4-6), eviscerate rat (7), perfused rat heart (8) and intact cat (9). However, slow penetration of a number of sugars into muscle of nephrectomized and eviscerated rats has now also been demonstrated, and this slow penetration is increased by insulin for D-lyxose, D-ribose, D-mannose, D-fructose and D-fucose, as well as for D-xylose, D-galactose and L-arabinose (10, 11). Although these results indicate that the concept of structural specificity in carbon atoms 1 to 3 for insulin responsiveness has proved to be too limited in scope, the lack of an effect of insulin upon intracellular entry of sorbitol, mannitol and raffinose is strong evidence that the action of insulin is not simply an acceleration of a process of physical diffusion (12).