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Am J Physiol Endocrinol Metab (June 7, 2005). doi:10.1152/ajpendo.00102.2005
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Submitted on March 9, 2005
Accepted on May 30, 2005

Impaired glucagon secretory responses in mice lacking the type 1 sulfonylurea receptor

Chiyo Shiota1, Jonathan V Rocheleau1, Masakazu Shiota1, David W Piston1, and Mark A Magnuson1*

1 Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA

* To whom correspondence should be addressed. E-mail: mark.magnuson{at}vanderbilt.edu.

Pancreatic {alpha}-cells, like {beta}-cells, express ATP-sensitive K+ (KATP) channels. To determine the physiological role of KATP channels in {alpha}-cells, we examined glucagon secretion in mice lacking the type 1 sulfonylurea receptor (Sur1). Plasma glucagon levels, which were increased in wild type mice after an overnight fast, did not change in Sur1 null mice. Pancreas perfusion studies showed that Sur1 null pancreata lacked glucagon secretory responses to hypoglycemia and to synergistic stimulation by arginine. Pancreatic {alpha}-cells isolated from wild type animals exhibited oscillations of intracellular free Ca2+ ([Ca2+]i) in the absence of glucose that became quiescent when the glucose concentration was increased. In contrast, Sur1 null {alpha}-cells showed continuous oscillations in [Ca2+]i regardless of the glucose concentration. These findings indicate that KATP channels in {alpha}-cells play a key role in regulating glucagon secretion, thereby adding to the paradox of how mice that lack KATP channels maintain euglycemia.




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