Exocrine pancreas mechanisms

Saliva and pancreatic juice both contain a-amylase. The activity of this enzyme in saliva is not significant compared with that in the pancreatic juice released into the gut. Release of amylase from the pancreas is controlled by a mechanism similar or identical to the one that stimulates the release of tr)rpsinogen, namely by the influence of CCK on the exocrine pancreas. Amylase catalyzes the hydrolysis of starch at interior positions rather than at the ends of the polymer. This activity yields products such as maltose and longer-chain-length oligomers of glucose. Also, amylase does not catalyze the hydrolysis of starches at branching points. Therefore, small branched-chain structures called dextrins are formed that are not hydrolyzed by the er zyme. 

Why this elaborate mechanism for getting active digestive enzymes into the gastrointestinal tract Synthesis of the enzymes as inactive precursors protects the exocrine cells from destructive proteolytic attack. The pancreas further protects itself against self-digestion by making a specific inhibitor, a protein called pancreatic trypsin inhibitor (p. 231), that effectively prevents... 

To further characterize the toxicity and investigate its possible mechanism, a 14-day time-course study in the rat was conducted to allow for the observation of the lesion development and progression (Brenneman et al., 2014). Light microscopic (i.e., histochemical and IHC with quantification) and ultrastructural (i.e., TEM) examination showed that the injury appeared to originate as degeneration and loss of endothelial cells in the capillaries at the exocrine-endocrine interface. This injury was not associated with any increases in traditional or exploratory serum biomarkers of exocrine injury nor any evidence of endocrine dysfunction as assessed via an OGTT however, it was associated with an increase in EMPs that was not pancreas specific. 

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