GI hormones Flashcards
Gastrin
Source: G cells (antrum of stomach) Action: increase H+, growth of gastric mucosa, motility
Regulation:
Increased by distention, alkalinzation, AA, peptides, vagal stimulation
Decreased by pH <1.5
High in ZES, chronic PPI
Phenylalanine and tryptophan are potent stimulators.
Cholecystokinin
Source: I cells (duodenum and jejunum) Action: increased pancreatic secretion, gallbladder contraction, gastric emptying, sphincter of oddi relaxation.
Regulation:
increase by FA and AA
CCK acts on neural muscarinic pathways to cause pancreatic secretion.
Secretin
Source: S cells (duodenum) Action: increased pancreatic bicarb secretion, decrease gastric acid secretion, increase bile secretion
Regulation: increased by acid, fatty ACID in lumen of duodenum.
Increased bicarb neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function.
Somatostatin
Source: D cells (pancreatic islets, GI mucosa)
Action:
decrease gastric acid/pepsinogen,
decrease pancreatic/small intestinal fluid secretion, decrease gallbladder contraction,
decrease insulin/glucagon
Regulation:
Increased by acid
Decreased by vagal stimulation
Inhibitory hormone, antigrowth hormone (inhibit digestion/abs of substances needed for growth)
Glucose-dependent insulinotropic peptide (GIP)
Source: K cells (duodenum, jejunum)
Action:
Exocrine: decrease gastric H+ secretion
Endocrine: increase insulin release
Regulation:
Increased by FA, AA, oral glucose.
This is why oral glucose is more rapidly used than IV.
Vasoactive intestinal polypeptide (VIP)
Source: parasympathetic ganglia in sphincters, gallbladders, small intestine.
Action:
Increase intestinal water and electrolyte secretion
Increase relaxation of intestinal smooth muscle/sphincter.
Regulation:
Increased by distention and vagal stimulation
Decreased by adrenergic output
VIPoma
Non alpha, beta islet cell tumor that secretes VIP
Copious Watery Diarrhea, Hypokalemia, and Achlorhydria (WDHA syndrome)
Nitric oxide
Action: increase smooth muscle, including lower esophageal sphincter.
Notes: loss of NO secretion is implicated in increased lower esophageal tone of achalasia
Motilin
Source: small intestine
Action: produces migrating motor complex (MMCs)
Regulation: increased in fasting state
Notes: motilin receptor agonist (erythromycin) used to stimulate intestinal peristalsis.
Intrinsic factor
Source: parietal cells (stomach)
Action: vitamin B12, binding protein required for uptake in terminal ileum
Autoimmune destruction of parietal cells;
chronic gastritis and pernicious anemia
Gastric acid
Source: parietal cells (stomach)
Action: decrease stomach pH
Regulation:
Increased by histmaine, ACh, gastrin
Decreased by somatostatin, GIP, prostagladin, secretin.
Pepsin
Source: chief cells (stomach)
Action: protein degradation
Regulation: increased by vagal stimulation, local acid
Note: inactive pepsinogen -> pepsin by H+
Bicarb
Source: mucosal cells (stomach, duodenum, salivary gland, pancreas) and Brunner’s gland (duodenum)
Action: neutralizes acid
Regulation:
Increased by pancreatic and biliary secretion with secretin
Notes: bicarb trapped in mucus that covers gastric epithelium.
Saliva
Secretion from parotid, submandibular, sublingual glands
Stimulates by sympathetic and parasympathetic
Amylase digests starch,
bicarb neutralizes bacterial acids,
mucin lubricates food
Normally hypotonic because of absorption but more isotonic with higher flow rates (less time for absorption)