The control of exocrine secretion of the acinar cells of the pancreas is via peptides, such as the hormones secretin and cholecystokinin, and somatostatin, which acts mainly as a paracrine factor, and via neurotransmitters.
The main hormones involved in stimulating secretion of pancreatic juice are secretin, which stimulates the secretion of the alkaline aqueous component, and cholecystokinin (CCK), which stimulates the secretion of the enzyme component. These hormones are produced in the duodenal mucosa in response to food constituents in duodenal chyme. As the secretion of pancreatic juice is under the control of two separate regulatory mechanisms, the composition of the juice can vary with regard to its enzyme protein content.
Somatostatin, which is present in the delta cells in the islets of Langerhan of the pancreas, is a powerful inhibitor of pancreatic secretion. It acts in a paracrine manner to inhibit the release of the exocrine alkaline and enzyme secretions, as well as the pancreatic hormones insulin and glucagons. In addition, somatostatin inhibits the release of a number of gastrointestinal hormones, including CCK, secretin and gastrin.
The nervous control of pancreatic secretions is via both sympathetic and parasympathetic nerves. Stimulation of cholinergic fibres in the vagus nerve enhances the rate of both alkaline and enzyme fluid. Stimulation of sympathetic nerves inhibits secretion owing to vasoconstriction of blood vessels in the gland, which leads to a decreased volume of juice secreted. At rest, the pancreas secretes enzymes at about 15% of the maximal rate and alkaline juice at less than 2%.
The control of secretion of pancreatic juice during a meal depends upon the volume and composition of the food ingested. Pancreatic secretions occur in the following three phases.
The sight or smell of food, or other sensory stimuli associated with the impending arrival of food, elicits increased pancreatic secretion via a conditioned reflex. The presence of food in the mouth stimulates secretion via a non-conditioned reflex. The control during this phase is therefore nervous and is mediated by impulses in cholinergic fibres in the vagus nerve. This results in a modest output of enzyme-rich pancreatic juice, containing very little bicarbonate.
The presence of food in the stomach stimulates the secretion of pancreatic juice via a hormonal mechanism. Activation of chemical receptors in the walls of the stomach causes the release of gastrin from G-cells into the local circulation. Distension of mechanoreceptors in the stomach also stimulates secretion. This phase results in a moderate production of pancreatic juice that is rich in enzymes but low in bicarbonate.
The intestinal phase is probably the most important phase in response to food. Food material in the duodenum stimulates both the alkaline and enzyme-rich components of pancreatic juice. The alkaline component of pancreatic juice is secreted in response to the presence of acid in the duodenum. Acid also stimulates the release of secretin from cells in the intestine and this hormone stimulates duct cells in the pancreas to secrete alkaline fluid. The enzyme-rich juice released during the intestinal phase is in response to fats and peptides in food. These cause the release of CCK from the walls of the duodenum into the bloodstream. CCK stimulates acinar cells to secrete enzymes. Trypsin in the duodenum inhibits the release of enzymes via the inhibition of CCK; this is a feedback control mechanism which limits the quantity of enzymes in the small intestine and may have a protective function.
In the absence of pancreatic enzymes, up to 35% of dietary fat and protein may be assimilated using less efficient pathways of digestion, such as salivary amylase and the enzymes for the brush border of the gut mucosa. It is estimated that pancreatic enzyme must fall below 10% of normal before maldigestion or malabsorption occurs.
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