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      Association of 1,5-Anhydroglucitol and 2-h Postprandial Blood Glucose in Type 2 Diabetic Patients

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          Abstract

          OBJECTIVE—To assess the association of 1,5-anhydroglucitol (1,5-AG) with 2-h postprandial glucose values in type 2 diabetic patients followed over 12 months in an outpatient setting.

          RESEARCH DESIGN AND METHODS—In 55 patients, we examined self-measured postprandial blood glucose values for correlations with 1,5-AG values over prespecified preceding time periods (3 days, 1 week, and weekly up to 12 weeks).

          RESULTS—The correlation coefficients for postprandial glucose values were −0.34 ( P < 0.05) for 3 days, −0.38 ( P < 0.001) for 1 week, and −0.40 ( P < 0.001) for 2 weeks preceding the measurement of 1,5-AG. Correlations declined for time periods >2 weeks before measurement of 1,5-AG. The correlation was lower with fasting/preprandial plasma glucose levels. There was no time dependency for the correlation between A1C and fasting or postprandial glucose.

          CONCLUSIONS—1,5-AG best reflected the 2-h postprandial glucose values of the 2 previous weeks.

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            1,5-anhydroglucitol and postprandial hyperglycemia as measured by continuous glucose monitoring system in moderately controlled patients with diabetes.

            Postprandial hyperglycemia is often inadequately assessed in diabetes management. Serum 1,5-anhydroglucitol (1,5-AG) drops as serum glucose rises above the renal threshold for glucose and has been proposed as a marker for postprandial hyperglycemia. The objective of this study is to demonstrate the relationship between 1,5-AG and postprandial hyperglycemia, as assessed by the continuous glucose monitoring system (CGMS) in suboptimally controlled patients with diabetes. Patients with type 1 or type 2 diabetes and an HbA(1c) (A1C) between 6.5 and 8% with stable glycemic control were recruited from two sites. A CGMS monitor was worn for two consecutive 72-h periods. Mean glucose, mean postmeal maximum glucose (MPMG), and area under the curve for glucose above 180 mg/dl (AUC-180), were compared with 1,5-AG, fructosamine (FA), and A1C at baseline, day 4, and day 7. 1,5-AG varied considerably between patients (6.5 +/- 3.2 mug/ml [means +/- SD]) despite similar A1C (7.3 +/- 0.5%). Mean 1,5-AG (r = -0.45, P = 0.006) correlated with AUC-180 more robustly than A1C (r = 0.33, P = 0.057) or FA (r = 0.38, P = 0.88). MPMG correlated more strongly with 1,5-AG (r = -0.54, P = 0.004) than with A1C (r = 0.40, P = 0.03) or FA (r = 0.32, P = 0.07). 1,5-AG reflects glycemic excursions, often in the postprandial state, more robustly than A1C or FA. 1,5-AG may be useful as a complementary marker to A1C to assess glycemic control in moderately controlled patients with diabetes.
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              Circulating 1,5-anhydroglucitol levels in adult patients with diabetes reflect longitudinal changes of glycemia: a U.S. trial of the GlycoMark assay.

              1,5-Anhydroglucitol (1,5AG) is a major circulating polyol arising primarily from ingestion and excreted competitively with glucose. Japanese studies have demonstrated reduced concentrations of 1,5AG in serum in hyperglycemic patients in comparison with euglycemic subjects and a gradual normalization of 1,5AG values for patients responding to antihyperglycemic therapies. In this first U.S. study, we assessed the ability of 1,5AG measurements to monitor glycemic control in a cohort of 77 patients with diabetes (22 with type 1 diabetes, 55 with type 2 diabetes) who presented with suboptimal glycemic control at baseline (defined as HbA(1c) >or=7%). Each patient received therapies consisting of combinations of diabetes education, nutritional counseling, and addition or dose adjustment of various insulins or oral antihyperglycemic medications. Therapy was targeted to reduce mean HbA(1c) by >or=1.0% over the monitoring period. 1,5AG, HbA(1c), fructosamine, and random glucose measurements were performed at baseline and at 2, 4, and 8 weeks after the initiation of therapy. 1,5AG, fructosamine, and glucose values progressed significantly toward euglycemia by week 2 of monitoring (Wilcoxon's signed-rank test, P < 0.05), with median changes of 93, -7, and -13% for 1,5AG, fructosamine, and glucose, respectively. In contrast, HbA(1c) values did not respond significantly to therapy until week 4. On an individual patient basis, 89.6% of patients displayed longitudinal changes of 1,5AG from baseline to week 8 in concordance with HbA(1c). 1,5AG was also highly correlated with HbA(1c) and fructosamine (Spearman rho = -0.6459 and -0.6751, respectively; both P < 0.0001). We conclude that 1,5AG responds sensitively and rapidly to changes in glycemia and monitors glycemic control in accordance with established markers.
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                Author and article information

                Journal
                Diabetes Care
                diacare
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                August 2008
                : 31
                : 8
                : 1534-1535
                Affiliations
                [1 ]Division of Endocrinology, Diabetes, and Clinical Nutrition, University Hospital, Bern, Switzerland
                [2 ]Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland
                [3 ]Department of Internal Medicine, Cantonal Hospital, Olten, Switzerland
                [4 ]Institute of Clinical Chemistry, Kantonsspital, St. Gallen, Switzerland
                [5 ]Division of Endocrinology, Diabetes, and Clinical Nutrition, University Hospital, Basel, Switzerland
                Author notes

                Corresponding author: Christoph Stettler, christoph.stettler@ 123456insel.ch

                Article
                3181534
                10.2337/dc08-0385
                2494656
                18426859
                286f5b8d-2eb0-4b85-8aab-a701b685d5ad
                Copyright © 2008, American Diabetes Association

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

                History
                : 22 February 2008
                : 16 April 2008
                Categories
                Clinical Care/Education/Nutrition/Psychosocial Research

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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