To elucidate the value of using plasma 1,5-anhydro-D-glucitol (AG) as a marker of glycemic control in diabetic patients, the relationship between the plasma concentration of AG and glucosuria was examined in 152 patients with non-insulin-dependent diabetes mellitus (NIDDM). After recovery from the deterioration of glycemic control in NIDDM patients had started, AG began to increase day by day. The recovery of plasma AG showed a constant linear increase curve when excellent glycemic control was attained. The ordinary daily recovery rate of plasma AG was estimated to be 0.3 microgram/ml, which was independent of body weight, sex, age, the difference in treatment, the duration of diabetes, or the level of plasma AG among NIDDM patients. This rate decreased according to the increase in urinary glucose. When we calculated the decrease rate of plasma AG (delta AG), assuming 0.3 microgram/day to be the maximum increase rate in a day, we found a high correlation between delta AG and urinary glucose at almost all AG levels except the normal range and observed that plasma AG (A) times urinary glucose (G) was relatively constant. The formula A x G = 16 is a simple equation for rough estimation of urinary glucose from the plasma AG concentration in a stable glycemic-controlled NIDDM patient, and we call it the A.G index. The plasma AG also correlated significantly with fasting plasma glucose (r = -.810) and glycosylated hemoglobin (r = -.856) in the same stable glycemic-controlled NIDDM patients. Based on these observations, we propose that plasma AG can serve as a new marker that may provide sensitive and analytical information about glycemic control.

D-mannose is an essential monosaccharide constituent of glycoproteins and glycolipids. However, it is unknown how plasma mannose is supplied. The aim of this study was to explore the source of plasma mannose. Oral administration of glucose resulted in a significant decrease of plasma mannose concentration after 20 min in fasted normal rats. However, in fasted type 2 diabetes model rats, plasma mannose concentrations that were higher compared with normal rats did not change after the administration of glucose. When insulin was administered intravenously to fed rats, it took longer for plasma mannose concentrations to decrease significantly in diabetic rats than in normal rats (20 and 5 min, respectively). Intravenous administration of epinephrine to fed normal rats increased the plasma mannose concentration, but this effect was negated by fasting or by administration of a glycogen phosphorylase inhibitor. Epinephrine increased mannose output from the perfused liver of fed rats, but this effect was negated in the presence of a glucose-6-phosphatase inhibitor. Epinephrine also increased the hepatic levels of hexose 6-phosphates, including mannose 6-phosphate. When either lactate alone or lactate plus alanine were administered as gluconeogenic substrates to fasted rats, the concentration of plasma mannose did not increase. When lactate was used to perfuse the liver of fasted rats, a decrease, rather than an increase, in mannose output was observed. These findings indicate that hepatic glycogen is a source of plasma mannose.

No abstract

We have developed a fully enzymatic method to measure 1,5 anhydro-D-glucitol (1,5-AG) in serum through use of pyranose oxidase (PROD: EC 1.1.3.10), glucokinase (EC 2.7.1.2), and an ATP-regenerating system. In a previous report (Clin Chem 1989;35:2039-43) the glucose interfering with the measurement of 1,5-AG was removed with a minicolumn. In the method used here, glucokinase and an ATP-regenerating system efficiently convert glucose to the unreactive compound, glucose 6-phosphate, making the method selective for 1,5-AG. The hydrogen peroxide produced in the oxidation of 1,5-AG by PROD is detected with a standard enzymatic color-developing system. The within-run and day-to-day precision (CV) of this method was 0.52-1.29% and 1.17-4.48%, respectively. The correlation (r) between the results obtained with our proposed method (y) and those obtained with the mini-column method (x) was 0.998 (y = 1.007x + 0.493 mg/L; n = 100; Sy/x = 0.641 mg/L). This newly developed method allows quicker and easier measurement of serum 1,5-AG than previously described methods.

We have developed a simple method for determination of 1,5-anhydro-D-glucitol in plasma, based on use of pyranose oxidase (EC 1.1.3.10), an enzyme with specificity toward pyranoid compounds such as 1,5-anhydro-D-glucitol and glucose. Plasma samples deproteinized with trichloroacetic acid are passed through a two-layer mini-column packed with strongly basic anion (OH- form, the upper layer) and strongly acidic cation (H+ form, the lower layer) exchange resins. 1,5-Anhydro-D-glucitol is efficiently recovered in the flow-through fraction, which is almost devoid of other sugars that are sensitive to pyranose oxidase. The hydrogen peroxide formed in the enzymatic oxidation of 1,5-anhydro-D-glucitol is detected by a standard method utilizing an enzymatic color-developing system. The overall assay system is highly specific for 1,5-anhydro-D-glucitol. The correlation between results obtained in the present method (x) and in the gas-liquid chromatographic (GLC) method (y) was: y = 1.062x-0.293 mg/L (r = 0.997, n = 49, Sxy = 10.78 mg/L). Compared with GLC, our method is simpler in the sample treatment step and quicker in the measuring step. The precisions of the two methods are comparable.