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Diabetes 51:S381-S384, 2002
© 2002 by the American Diabetes Association, Inc.

Section 3: Beta-Cell Stimulus-Secretion Coupling: K+ ATP Channels and CA2+

Gliclazide Directly Inhibits Arginine-Induced Glucagon Release

Kenan Cejvan1, David H. Coy2, Jens Juul Holst3, Erol Cerasi4, and Suad Efendic1

1 Department of Molecular Medicine, Endocrine and Diabetes Unit, Karolinska Hospital and Institute, Stockholm, Sweden
2 Peptide Research Laboratories, Department of Medicine, Tulane Health Sciences Center, New Orleans, Louisiana
3 Department of Medical Physiology, University of Copenhagen, Panum Institute, Copenhagen, Denmark
4 Department of Endocrinology and Metabolism, Hadassah Medical Center, Jerusalem, Israel

Arginine-stimulated insulin and somatostatin release is enhanced by the sulfonylurea gliclazide. In contrast, gliclazide inhibits the glucagon response. The aim of the present study was to investigate whether this inhibition of glucagon release was mediated by a direct suppressive effect of gliclazide or was secondary to the paracrine effect of released somatostatin. To eliminate the paracrine effects of somatostatin, we first perfused isolated rat pancreata with a medium supplemented with 23% of the standard calcium content. Second, we perifused isolated rat islets with a novel and highly specific antagonist of type 2 somatostatin receptor, DC-41-33 (2 µmol/l), which fully antagonizes the suppressive somatostatin effect on rat A cells. Gliclazide (30 µmol/l) inhibited glucagon release by 54% in the perfusion experiments, whereas the somatostatin response was nearly abolished. In islet perifusions with DC-41-33, arginine-induced glucagon release was inhibited by 66%. We therefore concluded that gliclazide inhibits glucagon release by a direct action on the pancreatic A cell.


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Copyright © 2002 by the American Diabetes Association.