Summary.The urinary excretion of 1,5-anhydro-D-glucitol, a pyranoid polyol, in humans was studied. The plasma of nondiabetic human subjects contained high concentrations of this polyol (> 110 ~tmol/1), and there was a tendency for the 24-h excretion of it to become more variable in direct proportion to its plasma concentration. In contrast, diabetic patients showed lower plasma concentrations of this polyol, and the variation in the 24-h excretion of 1,5-anhydro-D-glucitol was especially notable among the patients with an extremely low plasma concentration of the polyol. This diabetic group showed a statistically significant correlation (p<0.01), between the urinary 1,5-anhydro-D-glucitol and urinary glucose. This correlation was more markedly demonstrated during a 100-g oral glucose tolerance test: parallel changes were observed in the concentrations of 1,5-anhydro-D-glucitol and glucose in the urine collected every hour after the glucose load. These observations led to the proposal that low plasma concentration of this polyol, which is observed in diabetes mellitus, may be the result of a frequent and/or prolonged high blood glucose concentration beyond the renal threshold for glucose excretion.Key words: 1,5-anhydroglucitol, urinary excretion, reabsorption, glucosuria, hyperglycaemia.A pyranoid polyol resembling glucose, 1,5-anhydro-Dglucitol (AG), is a humoral component in humans and other mammals [1][2][3][4][5][6][7][8][9][10][11][12]. The plasma AG concentration is specifically reduced in diabetes mellitus [10] and shows several dynamic properties which are advantageous as a clinical marker for diabetes mellitus. First, the extent of the plasma AG reduction is apparently correlated with the severity of diabetes mellitus, and strict metabolic control can reverse this reduction [11]. Second, AG undergoes very slow turnover in vivo [8,12], and its plasma concentration remains stable over a 24-h period, showing little acute response to fasting, food intake, and insulin administration [11]. Finally, AG also shows chemical and biochemical stability [12], and accordingly, we found no significant limitation on the storage and transport of plasma samples for AG determination. On the other hand, the utility of the plasma AG concentration as a clinical marker is certainly limited by a lack of metabolic knowledge: the origin and clearance mechanism of AG in humans have not yet been established. Recently, we demonstrated the primary role of renal AG reabsorption in AG retention in rats and mice [12]. That study also indicated a possibility that the diabetic plasma AG reduction is due to a decrease in renal AG reabsorption. In order to evaluate in humans the role of renal function in AG retention in the circulation, we measured the urinary AG and urinary glucose as well as the plasma AG and blood glucose.
Subjects and methods
SubjectsStudy 1. The amounts of AG and glucose in the blood and in a 24-h urine sample were determined for 11 non-diabetic volunteers and 30 diabetic patients, which included two patients with Typ...