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This version published online on April 20, 2006
Endocrinology, doi:10.1210/en.2005-1410
A more recent version of this article appeared on September 1, 2006
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Submitted on November 7, 2005
Accepted on April 13, 2006

Ablation of the glucagon receptor gene increases fetal lethality, and produces alterations in islet development and maturation

Patricia M. Vuguin*, Mamdouh H. Kedees, Lingguang Cui, Yelena Guz, Richard W. Gelling, Morris Nejathaim, Maureen J. Charron, and Gladys Teitelman

Dept of Pediatrics and Dept of Biochemistry, Albert Einstein College of Medicine, Bronx, NY, 10461; Dept of Anatomy and Cell Biology, SUNY- Downstate Medical Center, 450 Clarkson Ave, Brooklyn, NY 11203; Metabolex INC. 3876 Bay Center Place. Hayward, CA 94545

* To whom correspondence should be addressed. E-mail: vuguin{at}aecom.yu.edu.

Although glucagon plays a pivotal role in glucose homeostasis, its role in the regulation of fetal growth and maturation is poorly understood. These issues were examined in a line of mice with a global deletion of the glucagon receptor (Gcgr-/-), which are characterized by lower blood glucose levels, and by {alpha} and {delta} cell hyperplasia in adults (1). Ablation of Gcgr was deleterious to fetal survival; it delayed {beta} cell differentiation and perturbed the proportion of {beta} to {alpha} cells in embryonic islets. In adults, the mutation inhibited the progression of {alpha} cells to maturity, affected the expression of several {beta} cell specific genes and resulted in an augmentation of the {alpha}, {beta} and {delta} cell mass. This increase was due to an augmentation in both islet number and in the rate of proliferation of cells expressing glucagon or insulin. These findings suggest that glucagon participates in a feedback loop that regulates the proportion of the different endocrine cell types in islets, the number of islets per pancreas and development of the mature {alpha} cell phenotype.
Key words: glucagon signaling • fetal growth and survival • islet cell development/maturation




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