Vol 8, No 6 (2019)
Research paper
Published online: 2020-01-23

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Correlations between biomarkers of oxidative stress, glycemic control and insulin resistance in women with type 2 diabetes

Ali Khosrowbeygi12, Mahsa Gholami3, Parvin Zarei3, Bahman Sadeghi Sedeh4, Mohammad Reza Rezvanfar5, Mohammad Reza Rezvanfar6
Clin Diabetol 2019;8(6):277-283.


Background. The main characteristic of type 2 diabetes mellitus (T2DM) is hyperglycemia due to insulin resistance. Enhanced oxidative stress owing to increased oxygen free radicals and/or reduced antioxidant defense has very important roles in T2DM development and also most of its complications. The aim of the current study was to evaluate correlations between biomarkers of oxidative stress, glycemic control and insulin resistance in women with T2DM. Materials and methods. Seventy nine women with T2DM were included in the current study and fasting blood samples were collected. Hemoglobin A1c (HbA1c); glucose; oxidative stress biomarkers including malodialdehyde, 8-isoprostane, catalase and total antioxidant capacity (TAC) were measured. The adiponectin/leptin (A/L) ratio and the homeostasis model assessment of beta-cell function (HOMA-B) were calculated. The results were considered significant when the p-value was less than 0.05. Results. Serum levels of TAC showed a significant positive correlation with the A/L ratio (r = 0.261, p = 0.02). A significant negative correlation was observed between values of HbA1c and TAC (r = –0.300, p = 0.007). However, HbA1c correlated positively with 8-isoprostane (r = 0.236, p = 0.036). Values of HOMA-B correlated negatively with values of HbA1c (r = –0.327, p = 0.003). Serum levels of 8-isoprostane were significantly higher in obese (BMI > 30 kg/m2) women than in non-obese (BMI < 30 kg/m2) women (p = 0.032). Values of catalase (p = 0.022) and HOMA-B (p = 0.009) were significantly lower in women with HbA1c ≥ 7.6% compared with women with HbA1c < 7.6%. Conclusions. In summary, chronic hyperglycemia results in oxidative stress. This situation might lead to less beta cells function. In addition, low levels of the A/L ratio were associated with increased oxidative stress.

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  1. Rajput R, Mukherjee J, Ayyar V, et al. The impact of cardiovascular outcome trials on the choice of insulins in the management of type 2 diabetes mellitus: An expert review. Clinical Diabetology. 2018; 7(5): 234–246.
  2. Bigagli E, Lodovici M. Circulating oxidative stress biomarkers in clinical studies on type 2 diabetes and its complications. Oxid Med Cell Longev. 2019; 2019: 5953685.
  3. Hurrle S, Hsu WH. The etiology of oxidative stress in insulin resistance. Biomed J. 2017; 40(5): 257–262.
  4. Picu A, Petcu L, Ştefan S, et al. Markers of oxidative stress and antioxidant defense in romanian patients with type 2 diabetes mellitus and obesity. Molecules. 2017; 22(5).
  5. Hou X, Liu J, Song J, et al. Relationship of hemoglobin A1c with β cell function and insulin resistance in newly diagnosed and drug naive type 2 diabetes patients. J Diabetes Res. 2016; 2016: 8797316.
  6. Mahjoub S, Masrour-Roudsari J. Role of oxidative stress in pathogenesis of metabolic syndrome. Caspian J Intern Med. 2012; 3(1): 386–396.
  7. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2014; 37 Suppl 1: S81–S90.
  8. Mehmetoglu I, Yerlikaya FH, Kurban S. Correlation between vitamin A, E, coenzyme Q(10) and degree of insulin resistance in obese and non-obese subjects. J Clin Biochem Nutr. 2011; 49(3): 159–163.
  9. Al-Hakeim HK, Abdulzahra MS. Correlation between glycated hemoglobin and homa indices in type 2 diabetes mellitus: prediction of beta-cell function from glycated hemoglobin. J Med Biochem. 2015; 34(2): 191–199.
  10. Aebi H. Catalase in vitro. Methods Enzymol. 1984; 105: 121–126.
  11. Benzie IF, Strain JJ. The ferric reducing ability of plasma (FRAP) as a measure of "antioxidant power": the FRAP assay. Anal Biochem. 1996; 239(1): 70–76.
  12. Mihara M, Uchiyama M. Determination of malonaldehyde precursor in tissues by thiobarbituric acid test. Anal Biochem. 1978; 86(1): 271–278.
  13. Gupta V, Mishra S, Mishra S, et al. L:A ratio, insulin resistance and metabolic risk in women with polycystic ovarian syndrome. Diabetes Metab Syndr. 2017; 11 Suppl 2: S697–S701.
  14. Katz A, Nambi SS, Mather K, et al. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J Clin Endocrinol Metab. 2000; 85(7): 2402–2410.
  15. Jung CH, Rhee EJ, Choi JH, et al. The relationship of adiponectin/leptin ratio with homeostasis model assessment insulin resistance index and metabolic syndrome in apparently healthy korean male adults. Korean Diabetes J. 2010; 34(4): 237–243.
  16. Zarini GG, Exebio JC, Podesta C, Huffman FG. Association between HOMA-B and A1C levels in Haitian Americans with type 2 diabetes. FASEB J. 2012; 26(1 Supplement):869-869. http://www.fasebj.org/doi/abs/10.1096/fasebj.26.1_supplement.869.9.
  17. Lee DH, Blomhoff R, Jacobs DR. Is serum gamma glutamyltransferase a marker of oxidative stress? Free Radic Res. 2004; 38(6): 535–539.
  18. Koenig G, Seneff S. Gamma-Glutamyltransferase: a predictive biomarker of cellular antioxidant inadequacy and disease risk. Dis Markers. 2015; 2015: 818570.
  19. Khosrowbeygi A, Ahmadvand H. Positive correlation between serum levels of adiponectin and homocysteine in pre-eclampsia. J Obstet Gynaecol Res. 2013; 39(3): 641–646.
  20. Ren Y, Li Y, Yan J, et al. Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis. Sci Rep. 2017; 7(1): 3209.
  21. Frühbeck G, Catalán V, Rodríguez A, et al. Involvement of the leptin-adiponectin axis in inflammation and oxidative stress in the metabolic syndrome. Sci Rep. 2017; 7(1): 6619.