title: Does serum 1,5-anhydroglucitol establish a relationship between improvements in HbA1c and postprandial glucose excursions? Supportive evidence utilizing the differential effects between biphasic insulin aspart 30 and insulin glargine.
abstract: OBJECTIVE
  To investigate the relationship between changes in glycated haemoglobin (HbA(1c)) and postprandial glucose excursions on 1,5-anhydroglucitol (1,5-AG) in patients with Type 2 diabetes, utilizing the differential effects between biphasic insulin aspart 30 (BIAsp 30) or insulin glargine (IGlar) on postprandial glucose (PPG) levels.
  
  
  METHODS
  1,5-AG was measured using the GlycoMark assay at baseline and after 12 and 28 weeks in the INITiation of Insulin to reach HbA(1c) Target (INITIATE) study of 233 patients randomized to either BIAsp 30 or IGlar.
  
  
  RESULTS
  Baseline 1,5-AG was low and not significantly different (4.9 +/- 3.5 and 4.3 +/- 2.6 microg/ml in the BIAsp 30 and IGlar groups, respectively). After 28 weeks, the levels of 1,5-AG were higher in the BIAsp 30 than in the IGlar group (13.4 vs. 11.1 microg/ml, P = 0.008) and change from baseline was 25% greater with BIAsp 30 than IGlar (8.4 vs. 6.7 microg/ml, P = 0.011). 1,5-AG levels increased as a function of decreasing HbA(1c) or the average change in postprandial plasma glucose (PPG(ave)) with significant relationships for 1,5-AG/ HbA(1c) vs. HbA(1c) or 1,5-AG/PPG(ave )vs. PPG(ave) (both P < 0.0001), respectively.
  
  
  CONCLUSIONS
  As reported in previous publications, 1,5-AG reflects ambient glycaemic control and increases with reductions in HbA(1c) and postprandial glucose. The greater reductions in postprandial excursion achieved with BiAsp 30 compared with glargine were associated with greater increases in 1,5-AG. Even moderate elevations in HbA(1c) substantially lower 1,5-AG, suggesting that it can be most discriminating in identifying patients with excessive postprandial glucose excursions at HbA(1c) levels that approach the upper end of the normal range.
authors.affiliation: Novo Nordisk Inc, Princeton, NJ, USA. alnm@novonordisk.com
authors.forename: A C
authors.initials: AC
authors.lastname: Moses
authors.forename: P
authors.initials: P
authors.lastname: Raskin
authors.forename: N
authors.initials: N
authors.lastname: Khutoryansky
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D061265:Biphasic Insulins; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000378:metabolism; D016021:Epidemiologic Studies; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism*; D006801:Humans; D007004:Hypoglycemic Agents / Q000378:metabolism / Q000627:therapeutic use*; D007328:Insulin / Q000031:analogs & derivatives* / Q000378:metabolism / Q000627:therapeutic use; D061267:Insulin Aspart; D000069036:Insulin Glargine; D007336:Insulin, Isophane; D049528:Insulin, Long-Acting; D008297:Male; D008875:Middle Aged; D019518:Postprandial Period
chemical_list: D061265:Biphasic Insulins; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D061267:Insulin Aspart; D000069036:Insulin Glargine; D007336:Insulin, Isophane; D049528:Insulin, Long-Acting; C557564:insulin aspart, insulin aspart protamine drug combination 30:70