Hormonal response to a meal

Vivian Imbriotis | June 21, 2026

Cephalic phase

  • CNS anticipates meal \(\xrightarrow{vagus}\) ACh release
  • Stimulates G cell \(\to\) gastrin
  • Stimulates enterochromaffin-like cell \(\to\) histamine
  • Both stimulate parietal cells \(\to\) HCl release

Gastric phase

  • Gastric stretch + peptides \(\to\) G-cell \(\to\) gastrin release. Gastrin acts on...
  • Chief cell \(\to\) pepsinogen release (also directly stimulated by ACh)
  • Parietal cell \(\to\) HCl release
  • Antrum \(\to \ \uparrow\)contraction strength and frequency \(\to \ \uparrow\)gastric emptying

Intestinal phase

  • \(\downarrow\)pH in duodenum (requires alkalinization before accepting more material from stomach) \(\to\) S-cell \(\to\) secretin release \(\to \ \uparrow\)alkaline pancreatic juice secretion, delayed gastric emptying
  • Proteins and fats in duodenum \(\to\) I-cell \(\to\) CCK release \(\to\) GRID - gallbladder contracts, sphincter of oddi relaxes, increased pancreatic secretions, delayed gastric emptying
  • Once pH rises (duodenum ready for current chyme to leave and to accept more from stomach) \(\to\) Mo-cell \(\to\) motilin release \(\to\) increased gastric emptying, increased intestinal motility
  • As nutrients travel to jejunum and ileum \(\to\) GLP1 release \(\to\) satiety, \(\downarrow\)gastric emptying, insulin release potentiated
  • BGL rises \(\to\) insulin release from pancreatic \(\beta\) cells \(\to\) glucagon inhibited \(\to\) increased glycolysis, glycogenesis, lipid storage; decreased gluconeogenesis, glycogenolysis, fatty acid beta-oxidation.