Eur J Endocrinol
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DOI: 10.1530/eje.1.01868
European Journal of Endocrinology, Vol 152, Issue 3, 389-394
Copyright © 2005 by European Society of Endocrinology
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CLINICAL STUDY

Evidence for altered adipocyte function in polycystic ovary syndrome

E Carmina, F Orio1, S Palomba2, T Cascella1, R A Longo, A M Colao1, G Lombardi1 and R A Lobo3

Department of Clinical Medicine, University of Palermo, Palermo, Italy, 1 Department of Oncology and Molecular Endocrinology, Federico II University, Naples, Italy, 2 Department of Obstetrics and Gynecology, University Magna Grecia of Catanzaro, Catanzaro, Italy and 3 Department of Obstetrics and Gynecology, Columbia University, New York, New York, USA

(Correspondence should be addressed to R A Lobo, Department of Obstetrics and Gynecology, Columbia-Presbyterian Medical Center, 622 West 168th Street, PH-16, Room 69, New York 10032-3784, USA; Email: ral35{at}columbia.edu)

Background: Adipocytokines are produced by adipose tissue and have been thought to be related to insulin resistance and other health consequences. We measured leptin, adiponectin, and resistin simultaneously in women with polycystic ovary syndrome (PCOS) and age- and weight-matched controls. Our hypothesis was that these simultaneous measurements would help determine whether adipocytokine secretion is abnormal in PCOS independent of body mass and whether these levels are related to insulin resistance as well as other hormonal changes.

Methods: Fifty-two women with PCOS and 45 normal ovulatory women who were age- and weight-matched were studied. Blood was obtained for adipocytokines (leptin, adiponectin, and resistin) as well as hormonal parameters and markers of insulin resistance as assessed by the quantitative insulin-sensitivity check index. Body mass index (BMI) was stratified into obese, overweight, and normal subgroups for comparisons between PCOS and controls.

Results: Adiponectin was lower (P < 0.05) and resistin was higher (P < 0.05) while leptin was similar to matched controls. Breakdown of the groups into subgroups showed a strong body mass relationship for leptin with no changes in resistin although adiponectin was lower in PCOS, even controlling for BMI. In controls, leptin and adiponectin and leptin and resistin correlated (P < 0.05) but not in PCOS. In controls, all adipocytokines correlated with markers of insulin resistance but not in PCOS.

Conclusions: When matched for BMI status, decreased adiponectin in PCOS represent the most marked change. This alteration may be the result of altered adipose tissue distribution and function in PCOS but no correlation with insulin resistance was found.




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