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Gynecol Endocrinol. 2010 Mar;26(3):161-6. doi: 10.3109/09513590903247816.

Serum resistin and adiponectin levels in young non-obese women with polycystic ovary syndrome.

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Faculty of Medicine, Department of Endocrinology and Metabolism, Dicle University, Diyarbakir, Turkey.



Although polycystic ovary syndrome (PCOS) was described more than half a century ago, the underlying cause of PCOS is still unknown. The aim of our study was to evaluate whether serum resistin and adipocytokine levels alter and its changes relate with low grade inflammation in non-obese young women with PCOS.


Newly diagnosed 31 young non-obese women with PCOS (mean age 21.8 +/- 5.4 years; body mass index (BMI): 23.8 +/- 6.6 kg/m(2)) and 25 BMI- and age-matched, regular-cycling, healthy women (mean age 24.9 +/- 5.7 years; BMI: 23.1 +/- 5.8 kg/m(2)) were included the study Anthropometric measurements were evaluated. Resistin, adiponectin, glucose, insulin, hormone profiles, Lipoprotein (Lp)(a), high sensitive C reactive protein (hs-CRP), and homocysteine levels were measured in the beginning of oral glucose tolerance test. Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated.


Non-obese young women with PCOS had high adiponectin levels (28.01 +/- 6.47 ng/ml in PCOS vs. 23.89 +/- 7.70 ng/ml in control subjects, p = 0.034), whereas serum resistin levels were not significantly different compared with healthy controls (14.14 +/- 6.6 ng/ml in PCOS vs. 13.78 +/- 4.26 ng/ml in control subjects). There were no significant differences between two groups in terms of fasting insulin, Lp(a), homocysteine, and hs-CRP levels. Mean HOMA-IR value of patients with PCOS was similar with control subjects (1.93 +/- 0.73 in PCOS; 1.15 +/- 0.54 in control group).


Resistin levels did not change in non-obese young women with PCOS whereas adiponectin level in non-obese young women with PCOS was significantly higher than control subjects, perhaps, because of no insulin resistance. Circulating resistin levels may not be candidate to play a role in pathogenesis of PCOS without insulin resistance or obesity.

[Indexed for MEDLINE]

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