Impact of postprandial and fasting glucose concentrations on HbA1c in patients with type 2 diabetes.
AIM: This study aimed to assess the relative contributions of postprandial and fasting glucose concentrations to overall hyperglycaemia. METHODS: Patients with type 2 diabetes (n=973) carried out self-monitored blood glucose (SMBG) profiles on entry into the European Exenatide (EUREXA) trial. Glucose area under the curve was calculated for postprandial excursions (AUC(ppg)) and total daytime concentrations >6.1 mmol/L (AUC(total)), as well as for the percentage of glycaemia due to postprandial excursions (%(ppg)). In addition, OGTT scores were assessed for each patient. Results were evaluated according to defined HbA(1c) categories. RESULTS: There was a significant linear relationship between HbA(1c) and the derived variables of AUC(ppg), AUC(total) and %(ppg) (P<0.001 for each), with explained variance greatest for AUC(total) (r(2)=37.4%). AUC(ppg) increased only slightly up to an HbA(1c) of 7.0%, but showed a steeper increase in higher HbA(1c) categories. Also, the increase in AUC(total) with increasing HbA(1c) was much more pronounced. As a result, the postprandial glucose excursion as a proportion of total glucose (%(ppg)) decreased across HbA(1c) categories from 61.0% at HbA(1c)<6.5% to 22.0% at HbA(1c)≥9.0%. HOMA-IR remained virtually unchanged through all HbA(1c) categories, while HOMA-B showed no large changes up to HbA(1c) 7.0%, but then decreased at higher HbA(1c) values. The ΔI30/ΔG30 ratio decreased in the HbA(1c) 7.0-7.9% category, but did not change greatly at higher HbA(1c) categories. CONCLUSION: With increasing HbA(1c), there was a decrease in the contribution of postprandial hyperglycaemia to total glycaemia, and fasting hyperglycaemia became more important. This is consistent with impaired insulin release, particularly first-phase release, at higher HbA(1c) levels.[1]References
- Impact of postprandial and fasting glucose concentrations on HbA1c in patients with type 2 diabetes. Schernthaner, G., Guerci, B., Gallwitz, B., Rose, L., Nicolay, C., Kraus, P., Kazda, C. Diabetes Metab. (2010) [Pubmed]
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