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Experimental Diabetes Research
Volume 2010 (2010), Article ID 853176, 6 pages
http://dx.doi.org/10.1155/2010/853176
Research Article

Insulin-Induced Electrophysiology Changes in Human Pleura Are Mediated via Its Receptor

1Department of Physiology, Medical School, University of Thessaly, Mezourlo, P.O. Box 1400, New Buildings, 41100 Larissa, Greece
2Department of Histopathology, Larissa University Hospital, 411 10 Larissa, Greece
3Department of Cardiothoracic Surgery, Larissa University Hospital, 411 10 Larissa, Greece
4Department of Thoracic Diseases, Larissa University Hospital, 411 10 Larissa, Greece

Received 7 February 2010; Revised 16 June 2010; Accepted 2 July 2010

Academic Editor: Mark A. Yorek

Copyright © 2010 V. K. Kouritas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Insulin directly changes the sheep pleural electrophysiology. The aim of this study was to investigate whether insulin induces similar effects in human pleura, to clarify insulin receptor's involvement, and to demonstrate if glibenclamide (hypoglycemic agent) reverses this effect. Methods. Human parietal pleural specimens were mounted in Ussing chambers. Solutions containing insulin or glibenclamide and insulin with anti-insulin antibody, anti-insulin receptor antibody, and glibenclamide were used. The transmesothelial resistance ( ) was determined. Immunohistochemistry for the presence of Insulin Receptors (IRa, IRb) was also performed. Results. Insulin increased within 1st min ( ), when added mesothelially which was inhibited by the anti-insulin and anti-insulin receptor antibodies. Glibenclamide also eliminated the insulin-induced changes. Immunohistochemistry verified the presence of IRa and IRb. Conclusion. Insulin induces electrochemical changes in humans as in sheep via interaction with its receptor. This effect is abolished by glibenclamide.