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Molecular and Cellular Biology, August 2001, p. 5624-5630, Vol. 21, No. 16
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.16.5624-5630.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Preserved Pancreatic beta -Cell Development and Function in Mice Lacking the Insulin Receptor-Related Receptor

Tadahiro Kitamura,1 Yoshiaki Kido,1 Serge Nef,2 Jussi Merenmies,2 Luis F. Parada,2 and Domenico Accili1,*

Naomi Berrie Diabetes Center and Department of Medicine, College of Physicians & Surgeons of Columbia University, New York, New York 10032,1 and Center for Developmental Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-91332

Received 10 January 2001/Returned for modification 5 March 2001/Accepted 15 May 2001

Receptors of the insulin/insulinlike growth factor (IGF) family have been implicated in the regulation of pancreatic beta -cell growth and insulin secretion. The insulin receptor-related receptor (IRR) is an orphan receptor of the insulin receptor gene (Ir) subfamily. It is expressed at considerably higher levels in beta  cells than either insulin or IGF-1 receptors, and it has been shown to engage in heterodimer formation with insulin or IGF-1 receptors. To address whether IRR plays a physiologic role in beta -cell development and regulation of insulin secretion, we have characterized mice lacking IRR and generated a combined knockout of Ir and Irr. We report that islet morphology, beta -cell mass, and secretory function are not affected in IRR-deficient mice. Moreover, lack of IRR does not impair compensatory beta -cell hyperplasia in insulin-resistant Ir+/- mice, nor does it affect beta -cell development and function in Ir-/- mice. We conclude that glucose-stimulated insulin secretion and embryonic beta -cell development occur normally in mice lacking Irr.

* Corresponding author. Mailing address: Russ Berrie Science Pavilion, 1150 St. Nicholas Ave., New York, NY 10032. Phone: (212) 304-7393. Fax: (212) 304-7390. E-mail: da230{at}columbia.edu.

Molecular and Cellular Biology, August 2001, p. 5624-5630, Vol. 21, No. 16
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.16.5624-5630.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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