The term somatostatin was originally applied to the 14-aminoacid cyclic peptide that is secreted by the hypothalamus and that inhibits the production of growth hormone from the anterior pituitary gland.  Somatostatin is now known to be secreted from other parts of the central nervous system and from pancreatic delta cells.  Somatostatin secreted from pancreatic "delta cells" decreases the secretion of secretin, cholecystokinin, glucagon, insulin, and gastrin.  Somatostatinomas are rare pancreatic islet cell tumors that arise from delta cells.  Patients with somatostatinomas present with hyperglycemia or hypoglycemia, steatorrhea (excessive fat in the feces), and gallbladder stones.  Gallbladder stones form because of poor gallbladder contractility, which is secondary to inhibition of cholecystokinin release.

(Choices C and D)  Somatostatin decreases the release of glucagon as well as insulin.  However, the secretion of insulin is more profoundly inhibited than is glucagon; therefore, the net result is hyperglycemia.

(Choice A)  Steatorrhea results from the decreased secretion of secretin as well as a decrease in gastrointestinal motility.

(Choice E)  A decrease in gastrin release causes hypochlorhydria.

(Choice F)  As indicated above, somatostatin does decrease growth hormone secretion from the normal pituitary gland, and it does so in growth-hormone-secreting pituitary adenomas.  However, somatostatin cannot be used in clinical practice because of its extremely short half-life.  Somatostatin analogs (octreotide and lanreotide) have a longer plasma half-life and are available for clinical use.

Educational Objective:
Reduced gallbladder contractility, due to decreased cholecystokinin secretion, is responsible for biliary stones in patients with somatostatinoma.