Comparative Evaluation of Oxidative Stress in Type-2 Diabetes Mellitus in Relation to Controlled Vs Uncontrolled Diabetes
DOI:
https://doi.org/10.21276/apalm.2385Keywords:
Oxidative stress, Type 2 diabetes mellitus, HbA1c, malondialdehyde, FRAPAbstract
Background: Type 2 Diabetes Mellitus (T2DM) is associated with the production of excess free radicals which are not neutralised by available antioxidants thereby, leading to oxidative stress (OS). The extent of oxidative damage and resulting diabetic complications may be determined by the degree of hyperglycemia viz; controlled vs uncontrolled T2DM.
Aim: To evaluate and compare oxidative stress in T2DM patients with good glycemic control vs uncontrolled T2DM, by estimating malondialdehyde (MDA, index of lipid peroxidation), ferric acid reducing ability of plasma (FRAP as total antioxidant capacity, TAC).
Methods: The study included 50 healthy controls (Gp I) and 100 T2DM patients which were further divided into: Gp II having good glycemic control (HbA1c ≤ 7.0%) and Gp III with uncontrolled T2DM (HbA1c >7.0%)(n=50 each). Fasting & post-prandial plasma glucose, HbA1c, MDA, FRAP & hsCRP were estimated using standard methods.
Result: MDA was significantly higher and FRAP was significantly lower in T2DM patients as compared to healthy controls. Further, T2DM patients (Gp III) with uncontrolled hyperglycemia had higher degree of oxidative stress vs Gp II patients with good glycemic control. Moreover there was: i) A significant positive correlation between HbA1c & MDA (p<0.001),& ii) Significant negative correlation between HbA1c & FRAP and MDA & FRAP (p<0.001) in T2DM patients.
Conclusion: Oxidative stress in T2DM patients is directly proportional to the degree of hyperglycemia measured as HbA1c.Therefore it is important to maintain tight glycemic control in T2DM patients (HbA1c ≤ 7%), to decrease oxidative stress and thereby delay the onset of diabetic complications.
References
2. Obrosova IG, Van Huysen C, Fathallah L, Cao XC, Greene DA, Stevens MJ. An aldose reductase inhibitor reverses early diabetes-induced changes in peripheral nerve function, metabolism, and antioxidative defense. The FASEB Journal. 2002; 16: 123-125.
3. Maritim AC, Sanders RA, Watkins JB III.Diabetes,oxidative stress and antioxidants: A Review. J Biochem Mol Toxicol 2003;17:24-38.
4. Gaweł S, Wardas M, Niedworok E, Wardas P. Malondialdehyde (MDA) as a lipid peroxidation marker. Wiad Lek. 2004; 57(9-10):453-5.
5. Benzie IF, Strain JJ. The ferric reducing ability of plasma (FRAP) as a measure of “antioxidant powerâ€: the FRAP assay. Anal. Biochem. 1996; 239: 70-76.
6. Nathan DM, Turgeon H, Regan S. Relationship between glycated haemoglobin levels and mean glucose levels over time. Diabetologia. 2007; 50: 2239-44.
7. American Diabetes Association: Standard of Medical Care in Diabetes-2007. Diabetes Care. 2007; 30; S4- S41.
8. Trinder P. Enzymatic determination of glucose in blood serum. Annals of Clinical Biochem.1969; 6:24-27.
9. Sampson EJ, Baird MA, Burtis CA et al. A coupled-enzyme equilibrium method for measuring urea in serum: optimization and evaluation of the AACC study group on urea candidate reference method. Clin Chem 1980; 26: 816-26.
10. Cook JG. Association of clinical Biochemists' Scientific and Technical Committee. Factors influencing the assay of creatinine. Ann Clin Biochem 1975; 12: 219-32.
11. Allain CC. Enzymatic Determination of Total Cholesterol in Serum. Clin Chem. 1974; 20: 470 - 74.
12. Henry JB. Clinical Diagnosis and Management by Laboratory Methods, 18th ed. W.B. Saunders, Philadelphia, 1991; 9:204-211.
13. Burstein M, Scholnick HR, Morgin R. Rapid method for isolation of lipoproteins from human serum by precipitation with polyanions. J Lipid Res 1970; 11:1583-1586.
14. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem. 1972; 18:499-502.
15. Satoh K. Serum lipid peroxide in cerebrovascular disorders determined by a new colorimetric method. Clin Chim Acta1978; 90: 37-43.
16. Zhou J, Li H, Ran X, Yang W, Wang W, et al. Reference values for continuous glucose monitoring in Chinese subjects. Diabetes Care. 2009; 32:1188–93.
17. Anne L, Peters at al. A clinical approach for the diagnosis of diabetes mellitus. JAMA. 1996; 276:1246-52.
18. Ahmed N, Khan J, Siddiqui TS. Frequency of dyslipidaemia in type 2 diabetes mellitus in patients of Hazara division. Ayub Med Coll Abbottabad. 2008;20 (2):51-4.
19. Gupta S, Mehndiratta M, Kalra S, Kalra OP, Shulka R, Gambhir JK. Association of biomarkers of oxidative stress with the risk of chronic kidney disease in type 2 diabetes Mellitus in North Indian population. J Diabetic Complications. 2015; 29: 338-42.
20. Lau DC, Dhillon B, Yan H, Szmitko PE, Verma S. Adipokines: molecular links between obesity and atheroslcerosis. Am J Physiol: Heart Circulation Physiol. 2005; 288: H2031-41.
21. Sarinnapakorn V, Wanicagool W. Association between hsCRP and HbA1cin overweight T2DM female patients. J Med Assoc (Thai). 2013; 96 (Suppl 3): S 54-8.
22. Pawar SM, Tolanur SI, Lakshmi TM, et al. MDA & FRAP status in Diabetics with Coronary Heart Disease patients. JPBMS. 2011; 4(12):1-4.
23. Chavan VU, Melinkeri RR. Study of protein carbonyl group, nitric oxide and MDA (index of lipid peroxidation) as biomarkers of oxidative stress in type 2 diabetes mellitus. Natl J Community Med. 2013; 4:294-9.
24. Duman BS, Oeztuerk M, Yilmazer S, Hatemi H. Thiols, Malondialdehyde and Total antioxidant status in the Turkish Patients with Type 2 Diabetes Mellitus. Tohoku J Exp Med. 2003; 201(3); 147-155.
25. Ahmed FN, Naqvi FN, Shafiq F. Lipid peroxidation and serum antioxidant enzymes in patients with type 2 Diabetes Mellitus. Ann NY Acad Sci. 2006; 1084: 481-9.
26. Kalaivanam KN, Dharmalingam M, Marcus SR.Lipid peroxidation in Type 2 Diabetes mellitus. Int J Diab Dev Countries.2006;26:30-32.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2019 Aisha Beg, Rajesh Kumar Thakur, Rahul Saxena, Gladys Rai, Saurabh Srivastava, Jasvinder Kaur Gambhir
This work is licensed under a Creative Commons Attribution 4.0 International License.
Authors who publish with this journal agree to the following terms:
- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access at http://opcit.eprints.org/oacitation-biblio.html).