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Am J Physiol Endocrinol Metab (May 11, 2004). doi:10.1152/ajpendo.00423.2003
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Submitted on September 22, 2003
Accepted on May 5, 2004

Disruption of growth hormone receptor gene causes diminished pancreatic islet size and increased insulin sensitivity in mice

Jun-Li Liu1*, Karen T Coschigano2, Katie Robertson1, Mark Lipsett3, Yubin Guo1, John J Kopchick2, Ujendra Kumar1, and Ye Lauren Liu1

1 Fraser Laboratories, Department of Medicine, McGill University, Montreal, Quebec, Canada
2 College of Osteopapthic Medicine, Edison Biotechnology Institute and Department of Biomedical Sciences, Ohio University, Athens, OH, USA
3 Department of Surgery, McGill University, Montreal, Quebec, Canada

* To whom correspondence should be addressed. E-mail: jun-li.liu{at}mcgill.ca.

Growth hormone, acting through its receptor (GHR), plays an important role in carbohydrate metabolism and in promoting postnatal growth. GHR gene deficient (GHR-/-) mice exhibit severe growth retardation and proportionate dwarfism. In order to assess the physiological relevance of growth hormone actions, GHR-/- mice were used to investigate their phenotype in glucose metabolism and pancreatic islet function. Adult GHR-/- mice exhibited significant reductions in the levels of blood glucose and insulin, as well as insulin mRNA accumulation. Immunohistochemical analysis of pancreatic sections revealed normal distribution of the islets albeit significantly smaller in size. The average size of the islets found in GHR-/- mice was only 1/3 of that of wild-type littermates. Total {beta}-cell mass was reduced 4.5-fold in GHR-/- mice, significantly greater than their body size reduction. This reduction in pancreatic islet mass appears to be related to decreases in proliferation and cell growth. GHR-/- mice were different from human Laron syndrome in serum insulin level, insulin responsiveness, and obesity. We conclude that growth hormone signaling is essential for maintaining pancreatic islet size, stimulating islet hormone production and maintaining normal insulin sensitivity and glucose homeostasis.




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