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D-ribose, administered intravenously to normal subjects, disappears rapidly from blood, is sparingly excreted in urine, and produces a significant decrease in blood glucose levels. 1 " 4 C 14 -labeled ribose has been traced to glucose 3 ' 6 and CO 2 8 in man, presumably via metabolism over pentose phosphate pathways. 3 ' 5 In addition, this sugar is an efficient glycogen precursor in several mammals.*" 8 Ribose metabolism may be insulin dependent, since administration of this hormone enhances the removal of ribose from the blood stream. 3 On the other hand, insulin appears to have no effect on transport of this pentose into muscle cells."The hypoglycemic effect of ribose in normal subjects is a property shared by galactose, 10 but not by other pentoses 11 or fructose. 13 It is noteworthy in this regard that, of several monosaccharides tested, only glucose, galactose, and ribose stimulated the release of insulin from dog pancreas. 13 Ribose may possibly produce a diminution of hepatic glucose outflow. It has been suggested that ribose impairs hepatic glycogenolysis, since this pentose can inhibit phosphoglucomutase in vitro. 3 Segal and his co-workers observed decreased blood glucose levels following the intravenous administration of 20 gm. of ribose to three diabetic subjects. 1 Results in the present study, using larger doses of ribose given to patients with both mild and severe diabetes, confirm this finding and show in addition that several aspects of the metabolism of this pentose remain unaltered in the diabetic state. METHODSFive per cent solutions of D-ribose, obtained from Pfanstiehl Laboratories, Inc., Waukegan, Illinois, were prepared using sterile pyrogen-free water and were checked bacteriologically for sterility. Four mild adult diabetic and four severe juvenile-type diabetic patients From the U.S. Army Medical Research and Nutrition Laboratory, Fitzsimons Army Hospital, Denver, Colorado.were each given an intravenous infusion of ribose (40 or 50 gm.) administered at a constant rate over a onehour period following an overnight fast. Insulin was withheld for at least twenty-four hours before the test. Heparinized venous blood samples and timed urine collections were obtained prior to the infusion and at hourly intervals thereafter.Blood glucose was measured directly in blood filtrates prepared by the Somogyi method" using the prepared enzymatic reagent, Glucostat, Worthington Biochemical Corporation (glucose oxidase, horse-radish peroxidases, phosphate buffer, and O-dianisidine) as described by Saifer and Gerstenfeld. 15 Ribose added to glucose solutions had no influence on color development by this method.Ribose in blood was determined by the orcinol method following treatment of the filtrates with glucose oxidase (Pfanstiehl). 11 Nonesterified fatty acids (NEFA) in plasma were measured by the method of Dole. 10 Glucose and ribose were determined on diluted urine by the methods described for blood. However, prior to incubation with Glucostat, diluted urine samples were treated with ion exchange re...

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In the course of studies of possible metabolic effects of dextran infusions. a patient with chronic liver disease was given repeated infusions of dextran. A marked decrease in the concentration of serum proteins was observed, with a greater reduction in globulin than in albumin. Detailed studies were undertaken to confirm and evaluate these particular findings. For this purpose. 4 additional patients with liver disease and 8 patients convalescent from diseases other than liver disease were studied.One patient was given only a single infusion of dextran. 750 cc of 1274 dextran in water: the other 12 received daily infusions of 1000 cc of 676 destran in saline. Five of these 12 men were given infusions for 4 successive days, 4 for 5 days! one for 6 days. and 2 for 15 days. Other than prolonged bleeding time ( 1 ) . slightly prolonged one-stage prothrombin time. and minor headaches, no difficulties were encountered. Some patients gained as much as 3 kg of weight. but none developed overt edema, Serum proteins were measured daily in most cases by the method of Reinhold ( 2 ) , in which the globulins are precipitated by a sulfate-sulfite solution, and the protein in solution measured by the biuret reaction. On selected serums drawn both before and after dextran infusions the serum proteins were also checked by sulfate-sulfi t e precipitation and the analysis of supernatant nitrogen content by the Kjeldahl method. Filter paper electrophoresis was also used to check the partition of serum proteins, using the dye elution technique €or colorimetric quantitation of the bromphenol blue bound by each protein zone. Dextran" levels were measured by the turbidity method(3). In 3 of the liver disease patients serum cholinesterase (4), zinc turbidity ( 5). and thymol turbidity ( 6 ) were also measured. Methods.ResuEfs. $.'With repeated infusi tran. levels of dextran as high as 2.5 g % were found in the serum. Dextran was but slo\vly removed ; appreciable levels were still present in the serum 10 to 15 days after infusion. Hematocrilts and total serum protein concentrations changed inversely with the destran level. In general the sum of the concentrations of protein and dextran remained constant. and roughl_v equalled the total pro-5 0-SERUM 45; PROTEINS 40-ALBUMIN 35-GL3BULIN 30-GM % -2 5-20--.lo-ZINC 8-TUQBIDITY -* r T S 6m s -0 THYMOL 4-TUREIDITY 2--0-LV'TS

Six apparently normal young men received salt intakes of up to 540 mEq/day, or more, with free access to water. The five subjects who tolerated these high intakes drank enough water to maintain the sodium concentration in the 24-hour urine specimens at a mean of 268 mEq/l. with a range of means in the individual subjects of 240–295 mEq/l. Under these circumstances there was little change in the size of the body fluid compartments. The results indicate that there is a maximum physiological concentration of sodium in the urine, probably in the range of 270–290 mEq/l., which is similar to the ‘limiting isorrheic concentration’ described by Wolf. ( The Urinary Function of the Kidney. New York: Grune, 1950.) Submitted on July 16, 1959

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