Both the exocrine and endocrine portions of the pancreas respond to a multiplicity of extracellular signals and a variety of nutrients. The extracellular signals exert their effects via different signal transduction pathways to elicit secretion. Earlier work has demonstrated the dispersal of the islets throughout the exocrine pancreas, lying in close contact with acinar tissues since no rigid connective tissue capsule surrounds the islets. Morphological evidence and physiological data have indicated that the islet peptides insulin, glucagon and somatostatin can modulate the secretory effects of cholecystokinin-octapeptide (CCK-8) in the exocrine pancreas. Moreover, a number of clinical and experimental studies show that pancreatic exocrine function is altered in diabetes mellitus. However, neither this dysfunction has been fully characterized nor its mechanism precisely established.
In vitro studies performed in our laboratory suggest the existence of a potentiation between the islet peptides and the classical pancreatic secretagogues in the regulation of exocrine secretion in healthy rats, but this interaction is impaired when the animal is rendered diabetic.
The present article aims to review in both the normal and diabetic condition: i) The morphology of the pancreas and the distribution of peptidergic nerves and islet peptides in the gland. ii) The effect of islet peptides and their interaction with the peptide secretagogue CCK-8 on the exocrine pancreatic function, both in vitro and in vivo and iii) The possible mechanisms involved in the above interaction at the sight of the evidence.
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