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Diabetes 51:406-412, 2002
© 2002 by the American Diabetes Association, Inc.

Miniglucagon (Glucagon 19-29)

A Novel Regulator of the Pancreatic Islet Physiology

Stéphane Dalle1, Ghislaine Fontés1, Anne-Dominique Lajoix2, Laurence LeBrigand1, René Gross2, Gérard Ribes2, Michel Dufour1, Léo Barry1, Dung LeNguyen1, and Dominique Bataille1

1 Institut National de la Santé et de la Recherche Médicale, Montpellier, France
2 Unité Mixte de Recherche du Centre National de la Recherche Scientifique, Institut de Biologie, Montpellier, France

Miniglucagon, the COOH-terminal (19-29) fragment processed from glucagon, is a potent and efficient inhibitor of insulin secretion from the MIN 6 ß-cell line. Using the rat isolated-perfused pancreas, we investigated the inhibitory effect of miniglucagon on insulin secretion and evaluated the existence of an inhibitory tone exerted by this peptide inside the islet. Miniglucagon dose-dependently inhibited insulin secretion stimulated by 8.3 mol/l glucose, with no change in the perfusion flow rate. A concentration of 1 nmol/l miniglucagon had a significant inhibitory effect on a 1 nmol/l glucagon-like peptide 1 (7-36) amide-potentiated insulin secretion. A decrease in extracellular glucose concentration simultaneously stimulated glucagon and miniglucagon secretion from pancreatic {alpha}-cells. Using confocal and electron microscopy analysis, we observed that miniglucagon is colocalized with glucagon in mature secretory granules of {alpha}-cells. Perfusion of an anti-miniglucagon antiserum directed against the biologically active moiety of the peptide resulted in a more pronounced effect of a glucose challenge on insulin secretion, indicating that miniglucagon exerts a local inhibitory tone on ß-cells. We concluded that miniglucagon is a novel local regulator of the pancreatic islet physiology and that any abnormal inhibitory tone exerted by this peptide on the ß-cell would result in an impaired insulin secretion, as observed in type 2 diabetes.


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