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Oxford Centre for Diabetes, Endocrinology, and Metabolism (T.M.B., C.C., J.A.H.W., M.I.M.), Churchill Hospital, Oxford OX3 7LJ, United Kingdom; School of Life Sciences (M.H., N.P.G.), Oxford Brookes University, Oxford OX3 0BP, United Kingdom; Department of Radiology (S.J.G., C.A.), John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom; Department of Clinical Biochemistry (K.B., A.V.-P.), Addenbrookes Hospital, Cambridge CB2 0QQ, United Kingdom; and Institute of Reproductive and Developmental Biology (S.F.), Imperial College (Hammersmith Campus), London W12 0NN, United Kingdom
Address all correspondence and requests for reprints to: Dr. Tom Barber, Diabetes Research Laboratories, Oxford Centre for Diabetes, Endocrinology, and Metabolism, Churchill Hospital, Old Road, Head-ington, Oxford OX3 7LJ, United Kingdom. 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: The objective of the study was to explore the potential contribution of RBP4 and adiponectin in the etiology of PCOS and their relationships with specific fat depot measurements.
Design: This was a cross-sectional study.
Setting and Participants: Serum RBP4 and adiponectin levels were compared between 50 PCOS cases and 28 female controls (including 22 body mass index/fat mass-matched pairs) and correlated with specific fat depot (including visceral) axial magnetic resonance imaging cross-sectional area measurements. All subjects were of U.K. British/Irish origin.
Main Outcome Measure(s): Serum levels of RBP4 (automated immunonephelometric assay) and adiponectin [immunoassay: total and high molecular weight (HMW)]. Data are 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 [39.0 µg/ml (31.0, 49.0) vs. 41.6 µg/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 19.9 µg/ml (14.2, 27.8) vs. 25.8 µg/ml (17.7, 37.7), respectively, unadjusted P = 2.4 x 10–3; adjusted P = 0.10]. For the paired-sample analyzes, there were no differences in RBP4 (P = 0.09), total adiponectin (P = 0.06), HMW adiponectin (P =0.19), or HMW to 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 to total adiponectin ratio (r2 = –0.44, P = 1.3 x 10–3). 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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