Horm Metab Res 2011; 43(6): 380-385
DOI: 10.1055/s-0031-1273767
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Hypoxia Induces Apelin Expression in Human Adipocytes

K. Geiger1 , 2 , A. Muendlein1 , 2 , N. Stark1 , 2 , C. H. Saely1 , 2 , 3 , M. Wabitsch4 , P. Fraunberger5 , H. Drexel1 , 2 , 3 , 6
  • 1Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria
  • 2Private University of the Principality of Liechtenstein, Triesen, Principality of Liechtenstein
  • 3Department of Medicine and Cardiology, Academic Teaching Hospital Feldkirch, Feldkirch, Austria
  • 4Division of Pediatric Endocrinology and Diabetes, University of Ulm, Ulm, Germany
  • 5Medical Central Laboratories, Feldkirch, Austria
  • 6Drexel University College of Medicine, Philadelphia, USA
Further Information

Publication History

received 08.09.2010

accepted 23.02.2011

Publication Date:
29 March 2011 (online)

Abstract

Adipokines play a central role in the development of diseases associated with insulin resistance and obesity. Hypoxia in adipose tissue leads to a dysregulation of the expression of adipokines. The effect of hypoxia on the more recently identified adipokine apelin in human adipocytes is unclear. Therefore, we aimed at investigating the role of hypoxia on the expression of the adipokine apelin. Differentiated human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes were cultured under hypoxic conditions for varying time periods. A modular incubator chamber was used to create a hypoxic tissue culture environment (defined as 1% O2, 94% N, and 5% CO2). In addition, hypoxic conditions were mimicked by using CoCl2. The effect of hypoxia on the expression of the investigated adipokines was measured by real-time PCR and the secretion of apelin was quantified by ELISA. Induction of hypoxia significantly induced mRNA expression of leptin and apelin in differentiated SGBS adipocytes compared with the normoxic control condition. Expression of adiponectin was significantly decreased by hypoxia. In addition, the amount of secreted apelin protein in response to hypoxia was elevated compared to untreated cells. Furthermore, we could demonstrate that the observed hypoxia-induced induction of apelin mRNA expression is in the first phase dependent on HIF-1α. In our study, we could demonstrate for the first time that apelin expression and secretion by human adipocytes are strongly induced under hypoxic conditions and that the early response on hypoxia with apelin induction is dependent on HIF-1α.

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Correspondence

H. DrexelMD, FESC 

Full Professor of Medicine

Vorarlberg Institute for Vascular

Investigation and Treatment

(VIVIT)

Carinagasse 47

6800 Feldkirch

Austria

Phone: +43/5522/303 2600

Fax: +43/5522/303 7533

Email: vivit@lkhf.at

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