HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 289/4/E570    most recent 00102.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (11) Citing Articles via Google Scholar Google Scholar Articles by Shiota, C. Articles by Magnuson, M. A. Search for Related Content PubMed PubMed Citation Articles by Shiota, C. Articles by Magnuson, M. A.

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

Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee

Submitted 9 March 2005 ; accepted in final form 30 May 2005

Pancreatic -cells, like -cells, express ATP-sensitive K⁺ (K_ATP) channels. To determine the physiological role of K_ATP channels in -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 -cells isolated from wild-type animals exhibited oscillations of intracellular free Ca²⁺ concentration ([Ca²⁺]_i) in the absence of glucose that became quiescent when the glucose concentration was increased. In contrast, Sur1 null -cells showed continuous oscillations in [Ca²⁺]_i regardless of the glucose concentration. These findings indicate that K_ATP channels in -cells play a key role in regulating glucagon secretion, thereby adding to the paradox of how mice that lack K_ATP channels maintain euglycemia.

pancreatic -cell; adenosine 5'-triphosphate-sensitive potassium channel; sulfonylurea receptor 1; pancreas perfusion; glucagon

This article has been cited by other articles:

				E. Tuduri, L. Marroqui, S. Soriano, A. B. Ropero, T. M. Batista, S. Piquer, M. A. Lopez-Boado, E. M. Carneiro, R. Gomis, A. Nadal, et al. Inhibitory Effects of Leptin on Pancreatic {alpha}-Cell Function Diabetes, July 1, 2009; 58(7): 1616 - 1624. [Abstract] [Full Text] [PDF]

				N. Gustavsson, S.-H. Wei, D. N. Hoang, Y. Lao, Q. Zhang, G. K. Radda, P. Rorsman, T. C. Sudhof, and W. Han Synaptotagmin-7 is a principal Ca2+ sensor for Ca2+-induced glucagon exocytosis in pancreas J. Physiol., March 15, 2009; 587(6): 1169 - 1178. [Abstract] [Full Text] [PDF]

				I. Quesada, E. Tuduri, C. Ripoll, and A. Nadal Physiology of the pancreatic {alpha}-cell and glucagon secretion: role in glucose homeostasis and diabetes J. Endocrinol., October 1, 2008; 199(1): 5 - 19. [Abstract] [Full Text] [PDF]

				E. Tuduri, E. Filiputti, E. M. Carneiro, and I. Quesada Inhibition of Ca2+ signaling and glucagon secretion in mouse pancreatic {alpha}-cells by extracellular ATP and purinergic receptors Am J Physiol Endocrinol Metab, May 1, 2008; 294(5): E952 - E960. [Abstract] [Full Text] [PDF]