PDF
ePub
Citation
Print
Abstract
Background
It is known that chronic sustained hyperglycemia and its consequent oxidative stress causes diabetic complication in type 2 diabetes. It has been further proven that glycemic variability causes oxidative stress. The aim of this study is to measure the average daily risk range (ADDR)-index of glycemic variability, and to evaluate relevant variables.
Methods
We measured the blood glucose level of type 2 diabetic patients who were treated with multiple daily injections from January to July, 2008. The blood glucose levels were checked four times a day for 14 days and were conversed according to the ADRR formula. The degree of glycemic variability was categorized into non-fluctuation and fluctuation groups. We collected patient data on age, sex, duration of diabetes, body mass index, HOMAIR, HOMAβcell and HbA1c.
Results
A total of 97 patients were enrolled in this study. The mean age, duration of diabetes, HbA1c and mean ADRR were 57.6 ± 13.4, 11.5 ± 8.5 years, 10.7 ± 2.5%, and 26.6 ± 9.8, respectively. We classified 18.5% of the patients to the non-fluctuation group, and 81.5% to the fluctuation group. ADRR was significantly correlated with duration of diabetes, fasting and postprandial glucose, fructosamine, HbA1c and BMI and HOMAβcell. In addition, this study confirmed that BMI, HOMAβcell and HbA1c were ADRR-related independent variables.
Figures and Tables
Fig. 1
ADRR (Average daily risk range) distributions. A. Total patients. B. Good metabolic control group (HbA1c < 7%). C. Poor metabolic control group (HbA1c ≥ 7%).
Table 1
Clinical characteristics of total patients
CAD, Coronary artery disease; CAN, Cardiovascular autonomic neuropathy; CVD, Cerebral vascular disease; DM, Diabetes melltius; F, Female; FPG, Fasting plasma glucose; HOMAIR, Homeostasis Model Assessment-Insulin resistance; HOMAβcell, Homeostasis Model Assessment-beta cell; M, Male; PPG, Postprandial plasma glucose. All data are expressed as means ± SD.
Table 2
Comparisons of non-fluctuation and fluctuation group
All data are expressed as means ± SD; P < 0.05 was considered significant. CAD, Coronary artery disease; CAN, Cardiovascular autonomic neuropathy; CVD, Cerebral vascular disease; FPG, Fasting plasma glucose; HDL, High density lipoprotein; hs-CRP, High sensitivity C-reactive protein; HOMAIR, Homeostasis Model Assessment-Insulin resistance; HOMAβcell, Homeostasis Model Assessment-beta cell; LDL, Low density lipoprotein; PPG, Postprandial plasma glucose.
References
1. Evans JL, Goldfine ID, Maddux BA, Grodsky GM. Oxidative stress and stress-activated signaling pathways: A unifying hypothesis of type 2 diabetes. Endocr Rev. 2002. 23:599–622.
2. Puddu P, Puddu GM, Galletti L, Ceavero E, Muscari A. Mitochondrial dysfunction as an initiating event in atherogenesis: A plusible hypothesis. Cardiology. 2005. 103:137–141.
3. Brownlee M. Banting lecture 2004. The pathobiology of diabetic complications: a unifying mechanism. Diabetes. 2005. 54:1615–1625.
4. Rohlfing CL, Wiedmeyer HS, Little RR, England JD, Tennill A, Godstein DE. Defining the relationship between plasma glucose and HbA1c. Diabetes Care. 2002. 25:275–278.
5. American Diabetes Association. Standards of medical care in diabetes. Diabetes Care. 2006. 29:suppl 1. S4–S42.
6. Hirsch IB, Brownlee M. Should minimal blood glucose variability become the gold standard of glycemic control? Journal of Diabetes and Its Complication. 2005. 19:178–181.
7. Monnier L, Colette C. Glycemic variability: Should we and can we prevent it? Diabetes Care. 2008. 31:suppl 2. S150–S154.
8. Monnier L, Mas E, Ginet C, Michel F, Villon L, Cristol JP, Colette C. Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes. JAMA. 2006. 295:1681–1687.
9. Service FJ, Molnar GD, Rosevear JW, Ackerman E, Gatewood LC, Taylor WF. Mean amplitude of glycemic excursions, a measure of diabetic instability. Diabetes. 1970. 19:644–655.
10. Boris P, Linda A, Erik O, William C. Evaluation of a new measure of blood glucose variability in diabetes. Diabetes Care. 2006. 29:2433–2439.
11. Boris P, Linda A, Daniel J, William C. Symmetrization of the blood glucose measurement scale and its applications. Diabetes Care. 1997. 20:1655–1658.
12. Levy JC, Matthews DR, Hermans MP. Correct homeostasis model assessment (HOMA) evaluation uses the computer program. Diabetes Care. 1998. 21:2191–2192.
13. Gottsater A, Ryden-Ahlgren A, Szelag B, Hedblad B, Persson J, Berglund G, Wroblewski M, Sundkvist G. Cardiovascular autonomic neuropathy associated with carotid atherosclerosis in type 2 diabetic patients. Diabet Med. 2003. 20:495–499.
14. Ziegler D, Laux G, Dannehl K, Spuler M, Muhlen H, Mayer P, Gries FA. Assessment of cardiovascular autonomic function: age-related normal ranges and reproducibility of spectral analysis, vector analysis, and standard tests of heart rate variation and blood pressure responses. Diabet Med. 1992. 9:166–175.
15. Boulton AJ, Vinik AI, Arezzo JC, Bril Vera, Feldman EL, Freeman Roy. Diabetic Neuropathies: A statement by the American Diabetes Association. Diabetes Care. 2005. 28:956–962.
16. Diabetes Control and Complication Trial Research Group. The relationship of a glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the diabetes control and complication trial. Diabetes. 1995. 44:968–983.
17. Klein R. Hyperglycemia and microvascular disease in diabetes. Diabetes Care. 1995. 18:258–268.
18. Brownlee M. Biochemistry and molecular cell biology of diabetic complication. Nature. 2001. 414:813–820.
19. UK Prospective Diabetes Study (UKPDS) Group. UKPDS) Group: Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complication in patients with type 2 diabetes (UKPDS 33). Lancet. 1998. 352:837–853.
20. UK Prospective Diabetes Study (UKPDS) Group. UKPDS) Group: Effect of intensive blood glucose control with metformin on complication in overweight patients with type 2 diabetes(UKPDS 34). Lancet. 1998. 352:854–865.
21. Ohkubo Y, Kishikawa H, Araki E, Miyata T, Isami S, Motoyoshi S, Kojima Y, Furuyoshi N, Shichiri M. Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with NIDDM: a randomised prospective 6-year study. Diabetes Res Clin Pract. 1995. 28:103–117.
22. Thomas P, Frederick L. Postchallenge hyperglycemia in a national sample of U.S. adults with type 2 diabetes. Diabetes Care. 2001. 24:1734–1738.
23. Ceriello A. The post-prandial state and cardiovascular disease: relevance to diabetes mellitus. Diabetes Metab Res Rev. 2000. 16:125–132.
24. Heller SR. Minimizing hypoglycemia while maintaining glycemic control in diabetes. Diabetes. 2008. 57:3177–3183.
25. Cryer PE. The Barrier of hypoglycemia in diabetes. Diabetes. 2008. 57:3169–3176.
26. Ceriello A, Esposito K, Piconi L, Michael A, Jessica E. Oscillating glucose is more deleterious to endothelial function and oxidative stress than mean glucose in normal and type 2 diabetic patients. Diabetes. 2008. 57:1349–1354.
27. Schlichtkrull J, Munck O, Jersild M. The M-value, an index of blood-sugar control in diabetics. Acta Med Scand. 1965. 177:95–102.
28. Ryan EA, Shandro T, Green K, Paty BW, Senior PA, Bigam D, Shapiro AM, Vantyghem MC. Assessment of the severity of hypoglycemia and glycemic lability in type 1 diabetic subjects undergoing islet transplantation. Diabetes. 2004. 53:955–962.
29. George D. Assessing glycemic control with self-monitoring of blood glucose and Hemoglobin A1c measurements. Mayo Clin Proc. 2007. 82:229–236.
30. Bonora E, Formentini G, Calcaterra F, Bonadonna RC, Lombardi S, Muggeo M, Bonfante N. Plasma glucose levels throughout the day and HbA1c interrelationship in type 2 diabetes. Diabetes Care. 2001. 24:2023–2029.
31. Rachel D, Gerald A, Elizabeth G, Christopher D. Is HbA1c affected by glycemic instability? Diabetes Care. 2003. 26:2728–2733.
32. Vinik AI, Maser RE, Mitchell BD, Freeman R. Diabetic autonomic neuropathy. Diabetes Care. 2003. 26:1553–1579.
XML Download