The concentration of 1-deoxyglucose(1,5-anhydroglucitol) in plasma from patients with insulin-dependent diabetes mellitus was measured by gas-liquid chromatography with an all-glass capillary column. Twenty-one plasma samples were obtained from 21 patients before insulin therapy, and 34 more from 13 patients receiving insulin therapy. 1-Deoxyglucose was generally not detectable in plasmas of diabetic patients before they received insulin; it was measurable in the patients who had received insulin, although its concentration was low compared with that of healthy subjects. We therefore suggest that the absence of 1-deoxyglucose in plasma is one of the markers of metabolic states of diabetes, perhaps reflecting a disturbed function of carbohydrate metabolism; its presence in plasma within a normal range may reflect the better control of diabetic patients.

1-Deoxyglucose (1,5-anhydroglucitol), a metabolite related to diabetes mellitus, was identified in human plasma by gas-liquid chromatography and by gas-liquid chromatography/mass spectrometry. Plasma polyols were accurately determined with a gas-liquid chromatograph equipped with an all-glass capillary column. The plasma content of 1-deoxyglucose in healthy persons varies with age. Although the precise physiological role of 1-deoxyglucose remains obscure, the method described here for determining the minor polyol components of plasma, as well as the findings of 1-deoxyglucose in the plasma of healthy subjects, may be useful for investigating the metabolic roles of 1-deoxyglucose.

Background: The association of glycated albumin (GA) with mortality is unclear in chronic hemodialysis patients with diabetes. We investigated the usefulness of GA by comparing it with hemoglobin A1c (HbA1c) in this patient population. Research design and methods: This was a multi-center, prospective cohort study of 841 Japanese chronic hemodialysis patients with diabetes. There were 235 women and 606 men included, with a mean age of 64 years. The primary and secondary endpoints were the incidence of all-cause and cause-specific mortality, respectively. The hazard ratios of GA and HbA1c for the endpoints were estimated using the values at baseline and during the study period. Results: During the mean follow-up period of 3.1 years, there were 184 deceased cases, in which 30 and 154 resulted from atherosclerotic cardiovascular disease (ASCVD) and non-ASCVD, respectively. The hazard ratio for a 1% increase in GA was 1.033 (95% confidence interval 1.006-1.060, p = 0.017) for all-cause mortality with a statistical significance when GA was treated as a time dependent variable, but not when the baseline levels or the mean levels during the followup period were used in the analysis (p = 0.815 and 0.517, respectively). GA was a significant predictor for ASCVD-related mortality in the above 3 models, but was not for non-ASCVD mortality. Higher levels of HbA1c were only associated with ASCVD-related mortality when HbA1c was treated as a time-dependent variable.

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