Abstract
The glycated albumin (GA) to HbA1c ratio (GA/HbA1c ratio) has been proposed as a marker of postprandial glucose excursion. The aim of this study was to explore the correlation between the GA/HbA1c ratio and beta cell function. Three hundred sixteen subjects with type 2 diabetes who had been admitted to our hospital were examined. Blood samples were obtained after fasting and 2 h after breakfast. Beta cell function was assessed by the serum C-peptide immunoreactivity (CPR) to plasma glucose ratio. Similarly, the correlation between the GA/HbA1c ratio and beta cell function was also estimated in 61 subjects with type 1 diabetes. As a result, the GA/HbA1c ratio was significantly correlated with the postprandial plasma glucose (r = 0.274, p < 0.001) and postprandial increment of plasma glucose (r = 0.269, p < 0.001), but not fasting plasma glucose level (r = 0.081, p = 0.15). Among HbA1c, GA and GA/HbA1c ratio, the GA/HbA1c ratio showed the highest correlation with beta cell function in subjects with type 2 diabetes (r = −0.455, p < 0.001). A robust association between beta cell function and the GA/HbA1c ratio was shown by multiple regression analysis adjusting for confounders. Similar correlations were also observed in subjects with type 1 diabetes. In conclusion, we confirmed a negative association between beta cell function and the GA/HbA1c ratio, a marker of postprandial glucose excursion, in this study using a relatively large sample size. These results indicate that beta cell dysfunction is associated with larger glucose excursions in subjects with both type 1 and type 2 diabetes.
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Abbreviations
- GA:
-
Glycated albumin
- CPR:
-
C-peptide immunoreactivity
- JDS:
-
Japan Diabetes Society
- GAD:
-
Glutamate decarboxylase
- IA-2:
-
Insulinoma-associated antigen-2
- IAA:
-
Insulin autoantibody
- FPG:
-
Fasting plasma glucose
- GFR:
-
Glomerular filtration rate
- SPIDDM:
-
Slowly progressive type 1 diabetes
References
Rhodes CJ. Type 2 diabetes-a matter of beta-cell life and death? Science. 2005;307:380–4.
Nathan DM, Kuenen J, Borg R, Zheng H, Schoenfeld D, Heine RJ. Translating the A1C assay into estimated average glucose values. Diabetes Care. 2008;31:1473–8.
Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HA. 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med. 2008;359:1577–89.
Nathan DM, Cleary PA, Backlund JY, et al. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. N Engl J Med. 2005;353:2643–53.
Patel A, MacMahon S, Chalmers J, et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med. 2008;358:2560–72.
Duckworth W, Abraira C, Moritz T, et al. Glucose control and vascular complications in veterans with type 2 diabetes. N Engl J Med. 2009;360:129–39.
Gerstein HC, Miller ME, Byington RP, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med. 2008;358:2545–59.
Monnier L, Mas E, Ginet C, et al. Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes. JAMA. 2006;295:1681–7.
Esposito K, Ciotola M, Carleo D, et al. Post-meal glucose peaks at home associate with carotid intima-media thickness in type 2 diabetes. J Clin Endocrinol Metab. 2008;93:1345–50.
Tominaga M, Eguchi H, Manaka H, Igarashi K, Kato T, Sekikawa A. Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. The Funagata Diabetes Study. Diabetes Care. 1999;22:920–4.
The DECODE Study Group on behalf of the European Diabetes Epidemiology Group. Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria. Arch Intern Med. 2001;161:397–405.
Nakagami T. Hyperglycaemia and mortality from all causes and from cardiovascular disease in five populations of Asian origin. Diabetologia. 2004;47:385–94.
Fukuda M, Tanaka A, Tahara Y, et al. Correlation between minimal secretory capacity of pancreatic beta-cells and stability of diabetic control. Diabetes. 1988;37:81–8.
Nakanishi K, Kobayashi T, Inoko H, Tsuji K, Murase T, Kosaka K. Residual beta-cell function and HLA-A24 in IDDM. Markers of glycemic control and subsequent development of diabetic retinopathy. Diabetes. 1995;44:1334–9.
Sassa M, Yamada Y, Hosokawa M, et al. Glycemic instability in type 1 diabetic patients: possible role of ketosis or ketoacidosis at onset of diabetes. Diabetes Res Clin Pract. 2008;81:190–5.
Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, Butler PC. Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes. Diabetes. 2003;52:102–10.
Selvin E, Francis LM, Ballantyne CM, et al. Nontraditional markers of glycemia: associations with microvascular conditions. Diabetes Care. 2011.
Yoshiuchi K, Matsuhisa M, Katakami N, et al. Glycated albumin is a better indicator for glucose excursion than glycated hemoglobin in type 1 and type 2 diabetes. Endocr J. 2008;55:503–7.
Imai T, Oikawa Y, Shimada A. Improved monitoring of the hyperglycemic state in type 1 diabetes patients by use of the glycoalbumin/HbA1c ratio. Rev Diabet Stud. 2007;4:44–8.
Koga M, Murai J, Saito H, Kasayama S. Glycated albumin and glycated hemoglobin are influenced differently by endogenous insulin secretion in patients with type 2 diabetes. Diabetes Care. 2010;33:270–2.
Wallace TM, Levy JC, Matthews DR. Use and abuse of HOMA modeling. Diabetes Care. 2004;27:1487–95.
The Commitee of the Japan Diabetes Society on the Diagnostic Criteria of Diabetes Mellitus. Report of the committee on the classification and diagnostic criteria of diabetes mellitus. J Diabetes Invest. 2010;1:212–28.
Saisho Y, Kou K, Tanaka K, et al. Postprandial serum C-peptide to plasma glucose ratio as a predictor of subsequent insulin treatment in patients with type 2 diabetes. Endocr J. 2011;58:315–22.
Goto A, Takaichi M, Kishimoto M, et al. Body mass index, fasting plasma glucose levels, and C-peptide levels as predictors of the future insulin use in Japanese type 2 diabetic patients. Endocr J. 2010;57:237–44.
Borg R, Kuenen JC, Carstensen B, et al. Associations between features of glucose exposure and A1C: the A1C-Derived Average Glucose (ADAG) study. Diabetes. 2010;59:1585–90.
Monnier L, Lapinski H, Colette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of type 2 diabetic patients: variations with increasing levels of HbA(1c). Diabetes Care. 2003;26:881–5.
Tahara Y, Shima K. Kinetics of HbA1c, glycated albumin, and fructosamine and analysis of their weight functions against preceding plasma glucose level. Diabetes Care. 1995;18:440–7.
Virtue MA, Furne JK, Nuttall FQ, Levitt MD. Relationship between GHb concentration and erythrocyte survival determined from breath carbon monoxide concentration. Diabetes Care. 2004;27:931–5.
Koga M, Matsumoto S, Saito H, Kasayama S. Body mass index negatively influences glycated albumin, but not glycated hemoglobin, in diabetic patients. Endocr J. 2006;53:387–91.
Koga M, Otsuki M, Matsumoto S, Saito H, Mukai M, Kasayama S. Negative association of obesity and its related chronic inflammation with serum glycated albumin but not glycated hemoglobin levels. Clin Chim Acta. 2007;378:48–52.
Koga M, Murai J, Saito H, Matsumoto S, Kasayama S. Effects of thyroid hormone on serum glycated albumin levels: study on non-diabetic subjects. Diabetes Res Clin Pract. 2009;84:163–7.
Kim MK, Kwon HS, Baek KH, et al. Effects of thyroid hormone on A1C and glycated albumin levels in nondiabetic subjects with overt hypothyroidism. Diabetes Care. 2010;33:2546–8.
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The authors thank Dr. Wendy Gray for editing the manuscript.
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Saisho, Y., Tanaka, K., Abe, T. et al. Glycated albumin to glycated hemoglobin ratio reflects postprandial glucose excursion and relates to beta cell function in both type 1 and type 2 diabetes. Diabetol Int 2, 146–153 (2011). https://doi.org/10.1007/s13340-011-0035-x
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DOI: https://doi.org/10.1007/s13340-011-0035-x