(Journal Article): Cholecystokinin Octapeptide: A Potential Growth Factor for Pancreatic Beta Cells in Diabetic Rats
 
Kuntz E, Pinget M, Damgé C (European Center for Study of Diabetes, Faculty of Medicine. Strasbourg, France, christiane.damge@medecine.u-strasbg.fr )
 
IN: JOP. J Pancreas (Online) 2004; 05(6):464-475

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ABSTRACT: CONTEXT: Diabetes is associated with the reduction of beta cell mass and activity. Cholecystokinin (CCK) is known to induce growth of the exocrine pancreas and to stimulate insulin secretion. OBJECTIVE: We investigated the possible role of CCK-octapeptide (CCK-8) in generating islet cell proliferation in type 1 and type 2 diabetic rats. METHODS: Streptozotocin-induced type 1 diabetic rats, streptozotocin/nicotinamide-induced type 2 diabetic rats and non-diabetic rats were subjected to CCK-8 (1, 2 and 4 microg/kg) or saline injections (for the control group), three times daily for 8 successive days. MAIN OUTCOME MEASURES: The islets of Langerhans were analyzed morphometrically; the beta-cell function was evaluated by an oral glucose tolerance test, and plasma basal glucose and insulin concentrations. RESULTS: In type 1 diabetic rats, CCK-8 induced an increase in beta cell surface associated with a marked increase in the mitotic index; this effect appeared at a concentration of 1 microg/kg CCK-8 and was the highest at a concentration of 4 microg/kg CCK-8. In addition, pancreatic- and plasma-insulin concentrations increased while fasting blood glucose concentrations were reduced when compared to saline-treated rats but the glycemic response to an oral glucose challenge did not significantly improve. In type 2 diabetic rats and in non-diabetic rats, CCK-8 treatment did not significantly affect either the structure or the functional state of beta-cells. CONCLUSIONS: CCK-8 could improve blood glucose concentrations in type 1 diabetic rats correlated with an increase in beta cell mass probably potentiated by the chronic hyperglycemic state.

TYPE OF PUBLICATION: Original Article