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Clinical Chemistry 0: clinchem.2004.043109v1, 2004; 10.1373/clinchem.2004.043109
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Received on September 16, 2004
Accepted on November 17, 2004

Endocrinology and Metabolism

Effect of Adiponectin Gene Polymorphisms on Circulating Adiponectin and Insulin Resistance Indexes in Women with Polycystic Ovary Syndrome

Nectaria Xita 1, Ioannis Georgiou 2, Anthoula Chatzikyriakidou 3, Maria Vounatsou 4, Gerasimos-Peter Papassotiriou 5, Ioannis Papassotiriou 5*, Agathocles Tsatsoulis 6

1 Department of Medicine, Division of Endocrinology, and These authors contributed equally to the study
2 Laboratory of Reproductive Genetics, University of Ioannina, Ioannina, Greece, and These authors contributed equally to the study
3 Laboratory of Reproductive Genetics, University of Ioannina, Ioannina, Greece
4 Blood Transfusion Service, "Henry Dunant" Hospital, Athens, Greece, and Department of Clinical Biochemistry, "Aghia Sophia" Children's Hospital, Athens, Greece
5 Department of Clinical Biochemistry, "Aghia Sophia" Children's Hospital, Athens, Greece
6 Department of Medicine, Division of Endocrinology

* To whom correspondence should be addressed. E-mail: biochem{at}paidon-agiasofia.gr and jpapasotiriou@ath.forthnet.gr.

Background: We examined the possible association of adiponectin gene polymorphisms with polycystic ovary syndrome (PCOS) and their influence on serum adiponectin and insulin resistance indexes in Greek women with PCOS.

Methods: We genotyped samples from 100 women with PCOS characterized with respect to body mass index (BMI), glucose and insulin concentrations during an oral glucose tolerance test (OGTT), lipid profile, and serum adiponectin concentrations and from 140 healthy controls for the 45T>G and 276G>T polymorphisms in the adiponectin gene.

Results: The distribution of genotypes and alleles of both polymorphisms was no different in women with PCOS and controls, indicating that the individual polymorphisms are not associated with increased risk for PCOS. However, the two polymorphisms were found to be associated with insulin resistance indexes among women with PCOS and to influence adiponectin production. In particular, carriers of the TG genotype at position +45 had greater hyperinsulinemia, as estimated by the area under the curve for insulin (AUCinsulin) during the OGTT, than those with the TT genotype (P <0.05), and this was independent of age and BMI. In addition, women with PCOS with the GG or GT genotypes at position +276 had a higher BMI (P = 0.01) and greater AUCinsulin (P = 0.01) than carriers of the TT genotype. The latter genotype was found less frequently among overweight/obese women with PCOS than in normal-weight individuals (P = 0.002). In addition, the presence of the GG or GT genotype was associated with lower serum adiponectin than the TT genotype, independent of age, BMI, and insulin concentrations (P = 0.03). Serum adiponectin was negatively correlated with serum triglycerides and insulin resistance indexes and positively with HDL-cholesterol.

Conclusions: Adiponectin gene polymorphisms at positions +45 and +276 are not associated with PCOS. However, these genomic variants may influence production of adiponectin and the metabolic variables related to insulin resistance/metabolic syndrome in patients with PCOS.


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