Format

Send to

Choose Destination
Exp Clin Endocrinol Diabetes. 2011 Jul;119(7):451-5. doi: 10.1055/s-0031-1279740. Epub 2011 Jun 10.

Insulin resistance in non-obese women with polycystic ovary syndrome: relation to byproducts of oxidative stress.

Author information

1
Institute of Endocrinology, Diabetes and Metabolic Diseases, Clinical Center of Serbia, University of Belgrade, Serbia.

Abstract

To get more insight into molecular mechanisms underlying oxidative stress and its link with insulin resistance, oxidative stress parameters, as well as, antioxidant enzyme activities were studied in young, non-obese women with polycystic ovary syndrome (PCOS). Study was performed in 34 PCOS women and 23 age and body mass index (BMI)-matched healthy controls. Plasma nitrotyrosine and malondialdehyde (MDA), representative byproducts of protein and lipid oxidative damage, were determined by enzyme immunoassay. Antioxidant enzyme activities, superoxide dismutase (SOD) and glutathione peroxidase (GPX) were studied spectrophotometrically. Insulin resistance was calculated using homeostasis assessment model (HOMA-IR). Plasma nitrotyrosine and MDA were increased, but only nitrotyrosine was significantly higher (p < 0.05) in PCOS women compared to controls. Uric acid (surrogate marker of × antine oxidase) was also significantly elevated in PCOS (p < 0.05). Both plasma SOD and GPX activity showed no statistically significant difference between PCOS and controls. Indices of insulin resistance (insulin and HOMAIR) were significantly higher in PCOS group and positively correlated with level of MDA (r = 0.397 and r = 0.523, respectively; p < 0.05) as well as GPX activity (r = 0.531 and r = 0.358, respectively; p < 0.05). Our results indicate that insulin resistance could be responsible for the existence of subtle form of oxidative stress in young, nonobese PCOS women. Hence, presence of insulin resistance, hyperinsulinemia and oxidative damage are likely to accelerate slow development of cardiovascular disease in PCOS.

PMID:
21667435
DOI:
10.1055/s-0031-1279740
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Georg Thieme Verlag Stuttgart, New York
Loading ...
Support Center