Retinol-Binding Protein 4 in Human Obesity

  1. Jürgen Janke1,
  2. Stefan Engeli1,
  3. Michael Boschmann1,
  4. Frauke Adams1,
  5. Jana Böhnke1,
  6. Friedrich C. Luft1,
  7. Arya M. Sharma2 and
  8. Jens Jordan1
  1. 1Franz-Volhard Clinical Research Center, Charité Campus Buch, and HELIOS Klinikum Berlin, Berlin, Germany
  2. 2Department of Medicine, McMaster University, Hamilton, Ontario, Canada
  1. Address correspondence and reprint requests to Stefan Engeli, MD, Franz Volhard Clinical Research Center (Haus 129), Charité Campus Buch, Wiltbergstr. 50, 13125 Berlin, Germany. E-mail: stefan.engeli{at}charite.de

Abstract

Studies in mice suggest that adipocytes serve as glucose sensors and regulate systemic glucose metabolism through release of serum retinol-binding protein 4 (RBP4). This model has not been validated in humans. RBP4 was highly expressed in isolated mature human adipocytes and secreted by differentiating human adipocytes. In contrast to the animal data, RBP4 mRNA was downregulated in subcutaneous adipose tissue of obese women, and circulating RBP4 concentrations were similar in normal weight, overweight, and obese women (n = 74). RBP4 was positively correlated with GLUT4 expression in adipose tissue, independent of any obesity-associated variable. Five percent weight loss slightly decreased adipose RBP4 expression but did not influence circulating RBP4. In another set of experiments, we stratified patients (n = 14) by low or high basal fasting interstitial glucose concentrations, as determined by the microdialysis technique. Venous glucose concentrations were similar throughout oral glucose tolerance testing, and basal RBP4 expression in adipose tissue and serum RBP4 concentrations were similar in the groups with higher and lower interstitial glucose levels. Our findings point to profound differences between rodents and humans in the regulation of adipose or circulating RBP4 and challenge the notion that glucose uptake by adipocytes has a dominant role in the regulation of RBP4.

Footnotes

  • J.Ja. and S.E. contributed equally to this work.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted July 10, 2006.
    • Received May 4, 2006.
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