Gut Peptide-Mediated Adaptive Response of the Exocrine Pancreas

Abstract

The gastrointestinal system is substantially involved in the regulation of exocrine pancreatic secretion, and it is therefore not surprising that intestinal diseases have been shown to affect exocrine pancreatic function. In rat experiments gastrectomy, truncal vagotomy, and subtotal colectomy stimulated pancreatic growth and altered pancreatic enzyme composition. Focusing on two main hormones supposed to be involved in the regulation of pancreatic adaptation, we studied basal and stimulated gastrin and cholecystokinin (CCK) pattern after the operative procedures. After total gastrectomy basal CCK values were unchanged, whereas postprandial CCK plasma values and the integrated postprandial CCK release were significantly increased. After subtotal colectomy CCK levels, both basal and postprandial, were significantly increased. In both of these conditions gastrin levels were either decreased (total gastrectomy) or unchanged (subtotal colectomy). CCK may therefore be the major humoral candidate to promote the observed pancreatic adaptive response. After truncal vagotomy CCK values remained unchanged, whereas basal and postprandial gastrin was significantly increased. Gastrin may be a candidate involved in the stimulation of pancreatic trophism after vagisection.

Key Words:

• Cholecystokinin
• gastric surgery
• gastrin
• pancreatic trophism
• rat