title: Impact of postprandial and fasting glucose concentrations on HbA1c in patients with type 2 diabetes.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Medicine I, Rudolfstiftung Hospital, Juchgasse 25, 1030 Vienna, Austria. guntram.schernthaner@wienkav.at
authors.forename: G
authors.initials: G
authors.lastname: Schernthaner
authors.forename: B
authors.initials: B
authors.lastname: Guerci
authors.forename: B
authors.initials: B
authors.lastname: Gallwitz
authors.forename: L
authors.initials: L
authors.lastname: Rose
authors.forename: C
authors.initials: C
authors.lastname: Nicolay
authors.forename: P
authors.initials: P
authors.lastname: Kraus
authors.forename: C
authors.initials: C
authors.lastname: Kazda
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001786:Blood Glucose / Q000032:analysis*; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000188:drug therapy; D000077270:Exenatide; D005215:Fasting; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis*; D006801:Humans; D006943:Hyperglycemia / Q000097:blood*; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000627:therapeutic use; D014688:Venoms / Q000627:therapeutic use
chemical_list: D001786:Blood Glucose; D000077270:Exenatide; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D010455:Peptides; D014688:Venoms