Primary Intestinal Tract Endocrine Hormones

Gastrin:  
         *Endocrine hormone, secreted by G-cells in antrum stomach mucosa
         *Stimulates secretion of gastric acids, lowers pH
         *Stimulates growth of gastric mucosa (cell-proliferative)
         *Exists in glycine-bound precursor in intercellular fluid (progastrin),
                the probable growth-stimulating factor
         *Stimulates pancreatic, gallbladder and small intestinal secretions
         *Diminished gastric acid, increased serum gastrin
         *Increased gastric acidity, decreased serum gastrin
         *Too much gastrin, stomach mucosa hyperplasia
         *enterochromaffin-like cells (ECL, found only in the acid-secreting
               stomach) proliferate in diminished acidity, dangerously so
               when inhibited by H2 blockers...even anticholinergics.
         *Infection with Helicobacter pylori causes hypergastrinemia, often
               causing gastric ulcer
         *Yeast metabolites (such as in beer or bread) stimulate gastrin
         *Normal gastrin response stimulates acquired immunity in gut
         *Diminished OR excessive levels impair normal resistance
Secretin: 
         *Endocrine hormone, secreted by cells in upper small-intestinal mucosa
         *Stimulates stomach enzymes, water and alkali secretions from pancreas
               and liver:  SUPPRESSES gastric acids
         *Complex meals stimulate the most; fluids and sugars the least
Somatostatin:
         *Paracrine/endocrine hormone (in the intestinal tract)
         *Made by D-cells in gastric mucosa
         *Suppresses gastric secretions; Gastrin rises, until suppressed by a
               combination of luminal acids and somatostatin
         *Infection with Helicobacter pylori causes somatostatin suppression,
               usually causing duodenal ulcer
         *Somatostatin also produced in small intestines and large intestines.
         *Somatostatin also produced in brain, and released by myenteric plexus
                cells
         *It inhibits motility and tone of stomach and small intestines and gall
               bladder, and inhibits formation of liver bile, but NOT bilirubin
         *It STIMULATES motility and tone of esophagus
         *It is elevated in blood and cerebrospinal fluids of obsessive-
               compulsives
         *It inhibits the release of ALL known GI hormones
         *It inhibits saliva, gastric, pacreatic, small intestinal and liver
               secretions
         *It inhibits splanchnic blood flow
         *It inhibits intestinal absorption
         *In the brain it inhibits somatotropin release by the hypothalamic/
               pituitary axis.
         *It is also secreted into the bloodstream by the hypothalamus, where
               it acts on the primary target tissues in the gut.
         *Like epinephrine, it is made LOCALLY (paracrine), and secreted
                SYSTEMICALLY (endocrine)
Bombesin  
         *A paracrine hormone in brain, it moderates blood flow (somehow)
         *It is an endocrine hormone, secreted from cells in the duodenum and
               jejunum.
         *It stimulates gastric ACID and pancreatic ENZYMES.
         *It stimulates contractions of the gall bladder and the biliary duct
         *It relaxes the common duct and sphincter of Oppy (see: Garfield)   
         *It strongly stimulates acquired immunity and antibody response in
                biliary apparatus AND duodenum/jejunum
         *It helps trigger Cholecystokinin release
         *It is a vasoconstrictor to breast arteries (??)
Cholecystokinin (CCK)
         *An endocrine hormone secreted by cells in the mucosa of the duodenum
               the jejunum, also (natch) by the hypothalamus
         *Meals stimulate CCK secretions by BOTH the gut and CNS simultaneously
         *It stimulates gall bladder contractions and pancreatic enzymes
         *Release of CCK GENERALLY satiates the appetite for more food.
         *Coincidentally, it is also the LAST major gut hormone secreted in a
               food cycle
         *A secondary rise of CCK (following the initial release) inhibits
               stomach motility and emptying, but NOT peristaltic action.
         *CCK can slow colon transit (unpredictable)
         *CCK has nor effect on small intestinal transit.
         *CCK is secreted MORE with unsaturated dietary fats than with saturated
               fats, and least of all with butterfats.
         *Coffee (intact or decaffeinated) increases intestinal CCK secretions.
         *Secretion stimulated by phenylalanine
         *It is part of the "antianalgesia response" in the spinal chord,
               following endorphin or opiate activity.
         *It is directly involved in opiate tolerance
         *CCK-4 (CCK-tetrapeptide) is associated, and may induce, panic states
         *CCK-8 (CNS) stimulates and modifies appetite for food
         *CCK-8 is VERY low in those with anorexia and/or bulimia
         *Anorectic/bulimics produce less gut CCK (usually CCK-4)
         *CCK is also a gut immuno-stimulant, but less active than gastrin and
               Bombesin (the most active)