Lipoperoxidation and antioxidant capacity in patients with poorly controlled type 2 diabetes

Abstract

Type 2 diabetes is a heterogeneous disease resulting from insulin resistance and/or from a β-cell secretory defect. Hyperglycemia, which occurs during type 2 diabetes, causes disorders of oxidative–antioxidative balance in the cells, leading to increased free-radical formation. Reduced antioxidant capacity is supposed to be one of the causes of the occurrence of complications in type 2 diabetes. The aim of this study was to evaluate lipoperoxidation and plasma antioxidant status in patients with poorly controlled type 2 diabetes with or without complications. In this study, 15 patients with type 2 diabetes without complications and 11 patients with type 2 diabetes with complications were enrolled. The ‘ferric-reducing ability of plasma’ showed no differences between the two experimental groups. A small, nonsignificant, Superoxide dismutase (SOD) activity reduction was observed in patients with diabetes with complications when compared to those patients with diabetes without complications; on the contrary, we found increased lipoperoxidation in patients with diabetes with complications compared with those patients with diabetes without complications. We also observed a positive correlation between malondialdehyde levels and high density lipoprotein or vitamin E in all analyzed patients with type 2 diabetes. Data obtained from our study show that patients with poorly controlled type 2 diabetes with complications have higher lipoperoxidation than patients with complication-free diabetes, although a residual compensatory response to hyperglycemia-induced oxidative stress occurs.

Keywords

diabetes HDL lipoperoxidation malondialdehyde SOD activity vitamin E

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References

Beauchamp C Fridovich I (1971) Superoxide dismutase: improved assays and an assay applicable to acrylamide gels. Anal Biochem 44: 276–287.

Benzie IF Strain JJ (1996) The ferric reducing ability of plasma (FRAP) as a measure of “antioxidant power”: the FRAP assay. Anal Biochem 239: 70–76.

Choi SW Benzie IF Lam CS Chat SW Lam J Yiu CH (2005) Inter-relationships between DNA damage, ascorbic acid and glycaemic control in Type 2 diabetes mellitus. Diabet Med 22: 1347–1353.

Colak E Majkić-Singh N Stanković S Srecković-Dimitrijević V Djordjević PB Lalić K (2005) Parameters of antioxidative defense in type 2 diabetic patients with cardiovascular complications. Ann Med 37: 613–620.

Feingold KR Grunfeld C Pang M Doerrler W Krauss RM (1992) LDL subclass phenotypes and triglyceride metabolism in non-insulin-dependent diabetes. Arterioscler Thromb 12: 1496–1502.

Flekac M Skrha J Hilgertova J Lacinova Z Jarolimkova M (2008) Gene polymorphisms of superoxide dismutases and catalase in diabetes mellitus. BMC Med Genet 9: 30–39.

George E Bieri JG (1983) Simultaneous determination of retinoland a-tocopherol in serum or plasma by liquid chromatography. Clin Chem 29: 708–712.

Kesavulu MM Rao BK Giri R Vijaya J Subramanyam G Apparao Ch (2001) Lipoperoxidation and antioxidant enzyme status in Type 2 diabetics with coronary heart disease. Diabetes Res Clin Pract 53: 33–39.

Lamarche B Tchernof A Moorjani S Cantin B Dagenais GR Lupien PJ (1997) Small dense low-density lipoprotein particles as a predictor of therisk of ischemic heart disease in men. Circulation 95: 69–75.

10.

Lodovici M Giovannelli L Pitozzi V Bigagli E Bardini G Rotella CM (2008) Oxidative DNA damage and plasma antioxidant capacity in type 2 diabetic patients with good and poor glycaemic control. Mutat Res 638: 98–102.

11.

Mateos R Lecumberri E Ramos S (2005) Determination of malondialdehyde (MDA) by high- performance liquid chromatography in serum and liver as a biomarker for oxidative stress. Application to a rat model for hypercholesterolemia and evaluation of the effect of diets rich in phenolic antioxidants from fruits. J Chromatogr B Analyt Technol Biomed Life Sci 827: 76–82.

12.

Meigs JB (2003) Epidemiology of cardiovascular complications in type 2 diabetes mellitus. Acta Diabetol 40: S358–S361.

13.

Meydani M (2004) Vitamin E modulation of cardiovascular disease. Ann N Y Acad Sci 1031: 271–279.

14.

Rolo AP Palmeira CM (2006) Diabetes and mitochondrial function: role of hyperglycemia and oxidative stress. Toxicol Appl Pharmacol 212: 167–178.

15.

Shepherd J (2007) Dyslipidaemia in diabetic patients: time for a rethink. Diabetes Obes Metab 9: 609–616.

16.

Sukalski KA Pinto KA Berntson JL (1993) Decreased susceptibility of liver mitochondria from diabetic rats to oxidative damage and associated increase in alpha-tocopherol. Free Radic Biol Med 14: 57–65.

17.

Tan HH Tan HK Lim HS Tan AS Lim SC (2002) Gestational diabetes mellitus: a call for systematic tracing. Ann Acad Med Singapore 31: 281–284.

18.

Turner RC Millns H Neil HAW Stratton IM Manley SE Matthews DR (1998) Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus: United Kingdom prospective diabetes study (UKPDS: 23). BMJ 316: 823–828.

19.

UK Prospective Diabetes Study (UKPDS) Group (1998) Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2diabetes (UKPDS 33). Lancet 12: 837–853.

20.

West IC (2000) Radicals and oxidative stress in diabetes. Diabet Med 17: 171–180.