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Submitted on December 17, 2007
Accepted on April 17, 2008
Oxford Centre for Diabetes, Endocrinology and Metabolism (T.M.B., C.C., F.K., J.A.H.W., M.I.M.), Churchill Hospital, Oxford OX3 7LJ, United Kingdom; School of Life Sciences, (M.H., N.G.), Oxford Brookes University, Oxford, OX3 0BP; Department of Radiology (C.A., S.J.G.), John Radcliffe Hospital, Oxford; Department of Clinical Biochemistry (K.B., A.V.P.), Addenbrooke's Hospital, Cambridge; Institute of Reproductive and Developmental Biology (S.F.), Imperial College (Hammersmith Campus), London W12 0NN, United Kingdom
* To whom correspondence should be addressed. E-mail: tom.barber{at}drl.ox.ac.uk.
Context: Insulin resistance, which associates with levels of retinol-binding protein 4 (RBP4) and adiponectin, is implicated in the development of polycystic ovary syndrome (PCOS).
Objective: To explore the potential contribution of RBP4 and adiponectin in the etiology of PCOS, and their relationships with specific fat depot measurements.
Design: A cross-sectional study.
Setting and participants: Serum RBP4 and adiponectin levels were compared between 50 PCOS cases and 28 female controls (including 22 BMI/fat mass-matched pairs), and correlated with specific fat depot (including visceral) axial MRI cross-sectional area measurements. All subjects were of UK British/Irish origin.
Main outcome measure(s): Serum levels of RBP4 (automated immunonephelometric assay) and adiponectin (immunoassay: total and high molecular weight [HMW]). Data reported as geometric mean [SD range], and optionally adjusted for fat mass and age.
Results: Between the 50 PCOS cases and 28 controls, serum RBP4 levels were indistinguishable (39.0µg/ml [31.0, 49.0] vs 41.6µg/ml [32.7, 52.9] respectively, unadjusted P=0.24; adjusted P=0.55). Total (and HMW) adiponectin levels were lower in PCOS cases (total adiponectin 19.9µg/ml [14.2, 27.8] vs 25.8µg/ml [17.7, 37.7] respectively, unadjusted P=2.4x10-3; adjusted P=0.10). For the paired-sample analyses, there were no differences in RBP4 (P=0.09), total adiponectin (P=0.06), HMW adiponectin (P=0.19) or HMW/total adiponectin ratio (P=0.98). In PCOS cases, L4-visceral fat area was associated positively with RBP4 (r2=0.34, P=0.01) and negatively with HMW/total adiponectin ratio (r2=-0.44, P=1.3x10-3). Controls showed similar relationships.
Conclusions: Although associated with visceral fat, serum RBP4 and adiponectin levels do not play important, fat-mass independent primary roles in the development of PCOS.
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