Association of 1,5-anhydroglucitol with cardiovascular disease and mortality

Elizabeth Selvin, Andreea Rawlings, Pamela Lutsey, Nisa Maruthur, James S. Pankow, Michael Steffes, Josef Coresh

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37 Scopus citations

Abstract

In diabetes, low concentrations of the biomarker 1,5- anhydroglucitol (1,5-AG) reflect hyperglycemic excursions over the prior 1-2 weeks. To the extent that hyperglycemic excursions are important in atherogenesis, 1,5-AG may provide independent information regarding cardiovascular risk. Nonetheless, few studies have evaluated associations of 1,5-AG with long-term cardiovascular outcomes in a population-based setting. We measured 1,5-AG in 11,106 participants in the Atherosclerosis Risk in Communities (ARIC) study without cardiovascular disease at baseline (1990-1992) and examined prospective associations with coronary heart disease (n = 1,159 events), ischemic stroke (n = 637), heart failure (n = 1,553), and death (n = 3,120) over 20 years of follow-up. Cox proportional hazards models were adjusted for demographic and cardiovascular risk factors. Compared with persons with 1,5-AG ≥6 μg/mL and no history of diabetes, persons with diabetes and 1,5-AG <6.0 μg/mL had an increased risk of coronary heart disease (HR 3.85, 95% CI 3.11-4.78), stroke (HR 3.48, 95% CI 2.66-4.55), heart failure (HR 3.50, 95% CI 2.93-4.17), and death (HR 2.44, 95% CI 2.11-2.83). There was a threshold effect, with little evidence for associations at "nondiabetic" concentrations of 1,5-AG (e.g., >10 μg/mL). Associations remained but were attenuated with additional adjustment for fasting glucose or HbA1c. These data add to the growing evidence for the prognostic value of 1,5-AG for long-term complications in the setting of diabetes.

Original languageEnglish (US)
Pages (from-to)201-208
Number of pages8
JournalDiabetes
Volume65
Issue number1
DOIs
StatePublished - Jan 2016

Bibliographical note

Funding Information:
This research was supported by National Institutes of Health (NIH)/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) grant R01-DK-089174 to E.S. E.S. was also supported by NIH/NIDDK grant K24-DK-106414. A.R. was supported by NIH/National Heart, Lung, and Blood Institute (NHLBI) grant T32-HL-007024. P.L. was supported by NIH/NHLBI grant R01-HL-103706. The ARIC study is carried out as a collaborative study supported by NHLBI contracts (HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C).

Publisher Copyright:
© 2016 by the American Diabetes Association.

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