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Am J Physiol Endocrinol Metab (March 13, 2007). doi:10.1152/ajpendo.00259.2006
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Submitted on May 29, 2006
Accepted on March 6, 2007

Impaired insulin secretion in a mouse model of Ataxia Telangiectasia

Philipp Miles1, Kai Treuner2*, Mark Latronica2, Jerrold M. Olefsky3, and Carrolee Barlow2

1 Department of Surgery, UCSD, San Diego, California, United States
2 BrainCells, Inc, San Diego, California, United States
3 Department of Medicine (0673), University of California-San Diego, La Jolla, California, United States

* To whom correspondence should be addressed. E-mail: ktreuner{at}braincellsinc.com.

Ataxia-Telangiectasia (A-T) is an autosomal recessive disease caused by mutations in the A-T mutated (ATM) gene. The gene encodes a serine/threonine kinase with important roles in the cellular response to DNA damage, including the activation of cell cycle checkpoints and induction of apoptosis. Although these functions might explain the cancer predisposition of A-T patients, the molecular mechanisms leading to glucose intolerance and diabetes mellitus (DM) are unknown. We have investigated the pathogenesis of DM in a mouse model of A-T. Here we show that young Atm-deficient mice show normal fasting glucose levels and normal insulin sensitivity. However, oral glucose tolerance testing revealed delayed insulin secretion and resulting transient hyperglycemia. Aged Atm-/- mice show a pronounced increase in blood glucose levels and a decrease in insulin and C-peptide levels. Our findings support a role for ATM in metabolic function and point toward impaired insulin secretion as the primary cause of diabetes mellitus in A-T.




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