Lecture 23: Intestinal Digestion + Absorption Flashcards
Ways of increasing intestinal surface area
Folds -> villi -> microvilli
Enterokinase
Aka enteropeptidase. Enterocyte brush border enzyme that cleaves + activates trypsinogen
Villi sloughing
Mucosal surface renews every 3-5 days; oldest cells are at the villi tips and slough off due to O2 deprivation. Newest cells are found in the crypts.
Intestinal villi counter-current effects
Arteriolar/venular proximity in the villus results in O2 loss to venous blood; creates hypoxia at villus tip leading to sloughing.
Carb digestion
Luminal salivary+pancreatic amylase digest carbs to maltose (di), maltotriose (tri), α/limited dextrins (poly/branch)
Then brush border disaccharidases produce mainly monosaccharides for absorption.
Almost all carbs absorbed before ileum.
Intestinal glucose absorption process
Primarily via active transport from lumen: Sodium-dependent glucose transporters (SGLT cotransport) powered by Na/H+ exchanger
Fructose facilitated diffusion
GLUT2 moves monosacc. into blood
Luminal protein digestion
Includes exogenous dietary + proteins from exocrine secretions/dying cells.
Stomach: pepsin -> oligopeptides/AAs
Intestine: pancreatic proteases + further oligopeptide digestion at brush border
Protein absorption
AAs + di/tripeptides absorbed; cytoplasm. peptidases break di/tripeptides and mostly free AAs are absorbed to blood (except Abs). Abt 15-20% protein not absorbed.
Standing osmotic gradient hypothesis
Water follows ions/solutes. When not eating, aquaporins absorb water. When eating, water goes to lumen then follows nutrients back in.
Ion/mineral absorption
- Apical sodium dependent transport of organic solutes
- Na absorbed w/ H+ exchange, extruded basolaterally w/ Na/K ATPase
- Na+/Cl- coupled absorption to secrete bicarb. for Cl- in
ENaC
Colonic epithelial Na+ channel, stimulated by aldosterone for Na+ and water resorption
Bicarb “absorption”
Facilitated by NHE.
Lumen H+ combines w/ bicarb; water remains in chyme, CO2 diffuses readily into cells and can then regen bicarb IC.
Ileal/colonic bicarb secretion function
Neutralizes SCFAs from bacteria; causes feces alkalinity.
Profuse diarrhea can cause metabolic acidosis.
K+ absorption
Mainly occurs via paracellular s. intestine pathways.
H2O absorption creates K+ absorption gradient.
Aldosterone -> colon K_ secretion due to Na+ absorption (some K loss in colon); diarrhea can lead to hypokalemia
Vitamin D and calcium absorption
Vitamin D3 upregulates apical channels, calbindin, basolateral Ca2+ ATPase to stimulate calcium
Iron absorption
- Vit. C + brush border ferric reductase (DCYTB) converts dietary Fe3+ to Fe2+; allows DMT1 transport
- Enterocyte ferritin binds IC Fe
- Export: hephaestin converts back to Fe3+
- Transferritin blood carrier
H2O/electrolyte secretion
- Occurs in intestinal crypts
- Na and K in w/ 2 Cl- in basolaterally -> apical Cl- secreted
VIP, ACh -> cAMP -> opens Cl- channels -> Na+, H2O follows into lumen (VIP = vasoactive intestinal peptide)
Cholera, pertussis toxins
