Background: Glycated albumin (GA) has been increasingly used as a reliable index for short-Term glycemic monitoring, and is inversely associated with b-cell function. Because the pathophysiologic nature of type 2 diabetes (T2D) is characterized by progressive decline in insulin secretion, the aim was to determine whether GA levels were affected by diabetes duration in subjects with T2D. Methods: To minimize the effect of glucose variability on GA, subjects with stably maintained HbA1c levels of ,0.5% fluctuation across 6 months of measurements were included. Patients with newly diagnosed T2D (n = 1059) and with duration.1 year (n = 781) were recruited and categorized as New-T2D and Old-T2D, respectively. Biochemical, glycemic, and C-peptide parameters were measured. Results: GA levels were significantly elevated in HbA1c-matched Old-T2D subjects compared to New-T2D subjects. Duration of diabetes was positively correlated with GA, whereas a negative relationship was found with C-peptide increment (DCpeptide). Among insulin secretory indices, dynamic parameters such as DC-peptide were inversely related to GA (r =20.42, p,0.001). Multiple linear regression analyses showed that duration of diabetes was associated with GA (standardized b coefficient [STDb] = 0.05, p,0.001), but not with HbA1c (STDb = 0.04, p,0.095). This association disappeared after additional adjustment with DC-peptide (STDb = 0.02, p = 0.372), suggesting that b-cell function might be a linking factor of close relationship between duration of diabetes and GA values. Conclusions: The present study showed that GA levels were significantly increased in subjects with longer duration T2D and with decreased insulin secretory function. Additional caution should be taken when interpreting GA values to assess glycemic control status in these individuals.
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© 2014 Lee et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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