I performed research on the relationship between exocrine and endocrine aspects of the pancreas, pancreatic exocrine functions in diabetes mellitus, the role of cholecystokinin (CCK) and its synthetic analogue on exocrine and endocrine pancreas function, the role of CCK on the pathogenesis of pancreatitis, the cellular mechanisms of reversible and irreversible pancreatitis, and pancreatic stellate cell activation.
This reduced basolateral exocytosis in part explained the less severe pancreatitis observed in Munc18c<sup>+/-</sup> mice after hyperstimulation with the CCK-8 analog caerulein.
Exogenous CCK administration has been used in animal models to study pancreatitis and also as a promoter of carcinogen-induced or Kras-driven pancreatic cancer.
However, the clinical relevance of CCK as a trigger factor has to be questioned, as it is difficult to envisage a situation in humans where abnormally high levels of CCK would be released into the circulation to trigger pancreatitis in alcoholics.
Cholecystokinin (CCK), which induces pancreatitis, stimulates CrkII tyrosine phosphorylation and CrkII protein complexes, raising the possibility it can be important in the acinar cell responses to ROS.
Impaired activation of pancreatic proteases in the small intestine is perceived as the pivotal problem that leads to continual feedback release of cholecystokinin, thus, in effect, causing a chronic hyperstimulation pancreatitis with intra-acinar activation of zymogens and, when bicarbonate secretion falls, precipitation of 'Reg' and other proteins in the duct system.