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Retinol-binding protein 4 is associated with insulin resistance, but appears unsuited for metabolic screening in women with polycystic ovary syndrome.

Möhlig M, Weickert MO, Ghadamgahi E, Arafat AM, Spranger J, Pfeiffer AF, Schöfl C

Department of Endocrinology, Diabetes and Nutrition, Charité-University Medicine Berlin, Campus Benjamin Franklin, 12200 Berlin, Germany.

OBJECTIVE: Adiposity, insulin resistance (IR), and hyperandrogenism are features of polycystic ovary syndrome (PCOS). Retinol-binding protein 4 (RBP4) secreted from adipose and liver tissues has been linked to IR. The impact of RBP4 on IR in PCOS and its usability to identify women with metabolic syndrome (MS) or impaired glucose tolerance ((IGT) or diabetes) were investigated. DESIGN: Plasma RBP4 was determined in 115 consecutive PCOS women. Associations with IR, body composition, and hyperandrogenemia were investigated by correlation and multiple linear regression analyses in 110 non-diabetics. Receiver operating characteristic curve analysis was used to evaluate RBP4 as a parameter for identifying MS and IGT or diabetes. RESULTS: RBP4 increased over tertiles of IR (P=0.009). RBP4 correlated with HOMA %S (R=-0.286, P= 0.002), waist-to-hip ratio (WHR) (R=0.233, P=0.034), and dual energy X-ray absorptiometry (DEXA)-lean body mass (R=0.282, P=0.016) but not with body mass index (BMI), DEXA-total or -trunk fat mass, hsCRP, free testosterone, DHEAS, androstenedione, and 17beta-estradiol. Adjusted for age, BMI, smoking, and IGT, the association between RBP4 and HOMA %S remained significant (P=0.032). RBP4 explained 4.6% of the variation in HOMA %S. RBP4 was higher in MS and IGT or diabetes, but its ability to identify these women was low (area under the curve, AUC=0.631, P=0.041 or AUC=0.660, P=0.016). CONCLUSIONS: In PCOS, RBP4 has a small independent impact on IR. It is not correlated with hyperandrogenemia, 17beta-estradiol, other adrenal steroids, or with markers of adiposity in general. Furthermore, RBP4 does not appear suitable for screening MS or impaired glucose metabolism (IGT or diabetes).

Published 25 March 2008 in Eur J Endocrinol, 158(4): 517-23.
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