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International Journal of Experimental Diabetes Research
Volume 2, Issue 2, Pages 101-112
http://dx.doi.org/10.1155/EDR.2001.101

Insulin and Glucagon Impairments in Relation with Islet Cells Morphological Modifications Following Long Term Pancreatic Duct Ligation in the Rabbit – A Model of Non-insulin-dependent Diabete

1Laboratoire de Physiopathologie Cellulaire, Université P. Sabatier, Toulouse III, 38, rue des 36 Ponts, Toulouse 31400, France
2Laboratoire de Pharmacologie de la Régulation, Université P. Sabatier, Toulouse III, 38, rue des 36 Ponts, Toulouse 31400, France
3Laboratoire de Biotogie Cellulaire et Molécutaire des Epithéliums, Université P. Sabatier, Toulouse III, 38, rue des 36 Ponts, Toulouse 31400, France

Received 16 August 2000; Accepted 21 February 2001

Copyright © 2001 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Plasma levels of glucose, insulin and glucagon were measured at various time intervals after pancreatic duct ligation (PDL) in rabbits. Two hyperglycemic periods were observed: one between 15–90 days (peak at 30 days of 15.1 ± 1.2mmol/l, p < 0.01), and the other at 450 days (11.2 ± 0.5 mmol/l, p < 0.02). The first hyperglycemic episode was significantly correlated with both hypoinsulinemia (41.8 ± 8pmol/l, r= –0.94, p < 0.01) and hyperglucagonemia (232 ± 21ng/l, r=0.95, p < 0.01). However, the late hyperglycemic phase (450 days), which was not accompanied by hypoinsulinemia, was observed after the hyperglucagonemia (390 days) produced by abundant immunostained A-cells giving rise to a 3-fold increase in pancreatic glucagon stores. The insulin and glucagon responses to glucose loading at 180, 270 and 450 days reflected the insensitivity of B- and A-cells to glucose. The PDL rabbit model with chronic and severe glycemic disorders due to the predominant role of glucagon mimicked key features of the NIDDM syndrome secondary to exocrine disease.