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

被引:11
作者
Moses, A. C. [1 ]
Raskin, P. [2 ]
Khutoryansky, N. [1 ]
机构
[1] Novo Nordisk Inc, Clin Dev Med & Regulatory Affairs, Princeton, NJ 08540 USA
[2] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA
关键词
basal; glycaemic control; insulin analogues; target; Type; 2; diabetes;
D O I
10.1111/j.1464-5491.2008.02384.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims 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 (R) 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 mu g/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 mu g/ml, P = 0.008) and change from baseline was 25% greater with BIAsp 30 than IGlar (8.4 vs. 6.7 mu g/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.
引用
收藏
页码:200 / 205
页数:6
相关论文
共 15 条
[1]  
BONORA E, 2001, DIABETOLOGIA, V46, pM9
[2]   Glycemic variability:: A hemoglobin A1c-independent risk factor for diabetic complications [J].
Brownlee, M ;
Hirsch, IB .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2006, 295 (14) :1707-1708
[3]   The pathobiology of diabetic complications - A unifying mechanism [J].
Brownlee, M .
DIABETES, 2005, 54 (06) :1615-1625
[4]  
Buse John B, 2003, Diabetes Technol Ther, V5, P355, DOI 10.1089/152091503765691839
[5]   Role of hyperglycemia in nitrotyrosine postprandial generation [J].
Ceriello, A ;
Quagliaro, L ;
Catone, B ;
Pascon, R ;
Piazzola, M ;
Bais, B ;
Marra, G ;
Tonutti, L ;
Taboga, C ;
Motz, E .
DIABETES CARE, 2002, 25 (08) :1439-1443
[6]   Postprandial hyperglycemia and diabetes complications - Is it time to treat? [J].
Ceriello, A .
DIABETES, 2005, 54 (01) :1-7
[7]   Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance - The STOP-NIDDM Ttrial [J].
Chiasson, JL ;
Josse, RG ;
Gomis, R ;
Hanefeld, M ;
Karasik, A ;
Laakso, M .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2003, 290 (04) :486-494
[8]   1,5-Anhydroglucitol and postprandial hyperglycemia as measured by continuous glucose monitoring system in moderately controlled patients with diabetes [J].
Dungan, Kathleen M. ;
Buse, John B. ;
Largay, Joseph ;
Kelly, Mary M. ;
Button, Eric A. ;
Kato, Shuhei ;
Wittlin, Steven .
DIABETES CARE, 2006, 29 (06) :1214-1219
[9]   Regression of carotid atherosclerosis by control of postprandial hyperglycemia in type 2 diabetes mellitus [J].
Esposito, K ;
Giugliano, D ;
Nappo, F ;
Marfella, R .
CIRCULATION, 2004, 110 (02) :214-219
[10]  
*GLYCOMARK, PACK INS