Differential mechanism and site of action of CCK on the pancreatic secretion and growth in rats.

Recent studies demonstrated that cholecystokinin (CCK) at physiological levels stimulates pancreatic enzyme secretion via a capsaicin-sensitive afferent vagal pathway. This study examined whether chemical ablation of afferent vagal fibers influences pancreatic growth and secretion in rats. Bilateral subdiaphragmatic vagal trunks were exposed, and capsaicin solution was applied.

Treatment for hyperglycemia promotes pancreatic regeneration in rats without CCK-1 receptor gene expression.

Introduction And Aim: Recent studies have suggested that CCK is not essential for normal pancreatic growth in mice. We examined whether the treatment of hyperglycemia participates in a non-CCK-1-receptor-mediated mechanism of pancreatic regeneration after partial (30%) pancreatectomy (Px) with use of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model for type 2 diabetes mellitus without CCK-1 receptor gene expression.

Methodology: Male OLETF rats were divided into five groups at 24 weeks of age.

Oleic acid-induced pancreatitis alters expression of transforming growth factor-beta1 and extracellular matrix components in rats.

Introduction And Aims: Extracellular matrix (ECM) components participate in the process of tissue repair and development of fibrosis in the pancreas. We studied the production kinetics of ECM components and transforming growth factor (TGF)-beta1 and identified their production sites in the pancreas following pancreatitis.

Methodology: Pancreatitis was induced in rats by a single intraductal infusion of oleic acid.