Pancreatic Secretion

There are two types of exocrine secretions produced by the pancreas.  Acinar cells produce digestive enzymes:  amylase, lipase, and peptidases.  Pancreatic peptidases are produced as inactive zymogens that are only activated after they reach the duodenum (see webpage on Zymogens).

ductThe other major secretion is bicarbonate (HCO3-), which is produced by the duct cells.  The bicarbonate acts to neutralize acidic chyme coming from the stomach.  As well, fluid that is produced by duct cells flushes enzymes and zymogens out into the large pancreatic duct.

At right is a picture from one of our histology slides.  The majority of exocrine tissue in the pancreas consists of acinar cells, which are the dark clusters visible throughout.  The pointer points to a small intercalated duct.  These ducts receive the acinar cell secretions, and secrete bicarbonate and fluid.  They connect to larger ducts that eventually lead to the large pancreatic duct that has its outlet at the duodenal papilla.


ductThe figure at left summarizes the regulation of pancreatic secretion.  A small amount of pancreatic secretion occurs due to neural inputs that are triggered by cephalic phase and gastric phase stimuli.  The majority of pancreatic secretion arises from intestinal phase stimuli (when chyme reaches the duodenum).  The hormones secretin and cholecystokinin (CCK) are released by endocrine cells that are located in the duodenal epithelium.  

As shown in the figure, secretin release is triggered by H+ ions (low pH).  Secretin then travels via the circulation to stimulate bicarbonate secretion by duct cells.  CCK release is triggered by digestive products (fats and peptides).  CCK then travels via the circulation to stimulate secretion by acinar cells.

Defect in duct cell secretion in cystic fibrosis

Secretion of bicarbonate by duct cells depends upon the protein CFTR. In the fall, we learned that CFTR is a chloride channel that provides the rate limiting step in fluid secretion in the small intestine (see webpage on Epithelial Transport).  But it turns out the CFTR protein is also a bicarbonate channel.  When the CFTR protein is defective, as it is in patients with cystic fibrosis, duct cell secretion is disrupted.  This causes a lack of fluid secretion to flush out pancreatic zymogens, blockage of pancreatic ducts, and inappropriate activation of trypsin in the pancreas.  The result is inflammation with damage to acinar and duct cells, which may be replaced by connective tissue. Patients with severe mutations of CFTR (little or no CFTR function) are often born with pancreatic insufficiency, meaning their pancreas does not release sufficient quantities of digestive enzymes.  They will have have a failure to thrive, and need to be treated with digestive enzyme supplements.  Less severe mutations in CFTR (with some channel function) still increase the risk for pancreatitis.  You can review the clinical effects of the CFTR mutation on the webpage Clinical Examples:  Epithelial Transport (from Fall Quarter).   



Quick Quiz


Fill in Answer Correct False Correct Answer
1. Fill in the blank.  The main stimulation of pancreatic secretion occurs during the [cephalic; gastric; intestinal] __________ phase.
2. Name the cell type responsible for bicarbonate secretion in the pancreas.
3. Where would you find an endocrine cell that releases the hormone CCK?
4. What protein is necessary for bicarbonate secretion in the pancreas?


(Spelling must be correct)