Absorption
Small intesine - 4m
Folds of Kerckring - 3x (controlled by muscularis mucosa)
Villi - 10x (network of arteries and veins)
Microvilli - 20x (brush border!!! bb enzymes finsish digestion)
Pathway of Nutrients
a nutrient must cross 8 barriers to be absorbed!
- unstirred layer
- glycocalyx
- apical cell membrane
- cytoplasm of enterocyte
- basolateral cell membrane
- intercellular space
- basement membrane
- wall of capillary/lymph vessel
Carb Digestion
begins in mouth - amylase breaks down starches to maltose –> Brush border enzymes furhter break down maltose, lactose and sucrose into glucose, galactose and fructose
dietary CHO - 40-60% starch, 30-40% suc/lac, 5-10% glu/fruc
nondigestable polymers = fiber (lignins, pectins, cellulose)
SGLT1 - Na+ and G or G bind (HAS to be a hexose/pyranose in D formation –> F will NOT bind)
- secondary active transport
GLUT5 - fructose receptor (facilitated diffusion via gradient)
SGLT2 - all sugars can exit!!! (Na exits via Na/K ATPase)
Protein Digestion
- gastric and pancreatic peptidases break down into AAs to be absorbed
- Pepsin = Proteins to proteoses/peptones/polypeptides
- Trypsin/Chymotrypsin/Carboxypeptidase/Proteolase = proteoses to polypeptides + AAs
- Peptidases = polypeptides + AAs to AAs
(Enteropeptidases are ALWAYS there but only active when trypsin comes in and cleaves)
- Endopeptidase - trypsin (basic aa), chymotrypsin (aromatic aa), elastase (neutral aa)
- Exopeptidase - carboxypeptidase A (aromatic/neutral/aliphatic AA), carboxypeptidase B (basic aa)
- INACTIVE FORMS? Add “pro” or “ogen”
gly/arg = basic
trp/try = aromatic
Abnormal Protein Assimilation
- Pancreatic Insufficiency
pancreatitis or cystic fibrosis (nitrogen in stool malabsorption)
- Congenital Absensce of Trypsin
babies can uptake whole protein because they don’t have trypsin/proteolytic enzymes! Phagocytosis due to underdevelopment
- Hartnup Disease
cannot absorb NEUTRAL AAs! –> can still be absorbed as di-/tri-peptides but requires oliogpeptide cotransporte
(CANT absorb phenylalanine)
Lipid Digestion
FA + glycerol to digest!
(most dietary fat = neutral fat or TGL)
- Emulsification
- Enzymatic Digestion (to get monoglyc + FA)
- Reconstitution of triglyceride and chylomicron formation
Pancreatic Lipase: TGL to monoglyceride + FA
Cholesterolester Hydrolase: FA + glycerol
Chylomicrons
Chylomicron = apoprotein + TGL
- formed in enterocyte and packaged by golgi
- secreted by exocytosis into interstitial space
- enter central lacteal of villi and transported to venous system via thoracic duct
- lipoprotein lipase works with apolipoprotein C to degrade TGL to FFA + glycerol within chylomicron
- Chylomicron remnant is phagocytized in hepatocytes
Intrinsic Factor + B12
B12 = cyanocobalamin (released by pepsin from food)
B12 deficiency –> pernicious anemia!
- Stomach - dietary B12 bound by B12 binding proteins in gastric juice
- Duodenum - pancreatic proteases digest binding protein, which releases B12 to bind to intrinsic factor (released by parietal cells)
- Ileum - intrinsic factor + vitamin B12 complex absorbed by endocytosis
- *** ONLY indispensible substance in gastric juice!
Sodium Absorption
Aldosterone increases Na+ reabsorption and K+ secretion in SI and colon!
- Nutrients? jejunum
- Alkaline lumen? jejunum (some duod)
- Electroneutral/electrogenic NaCl? Ileum, Colon
Chloride Absorption
- passive Cl- from lumen (-)? Jejunum & Colon
- Cl-/Bicarb echange? Proximal colon
- Electroneutral NaCL? Ileum & Colon
- Cl- secretion in crypts? duo/je/il/colon
Crypt Cell
secretion?
- cAMP activates Cl- channels
- Na+ follows electrical gradient
- H2O moves along osmotic gradient
- Cholera toxin increases cAMP levels IRREVERSIBLY
RESULT? increased cAMP! (Cl- leaves cell)
Diarrhea
4 types
- Secretory (cholera toxin)
- Osmotic (pancreatic disease, celiac, lactose intolerance, short bowel synd)
- Motility related (vagotomy, diabetic neuropathy)
- Inflammatory (infections, autoimmune - crohns)
“SOMI”
Cholera
cholera toxin stimulates secretion of water and electrolytes from crypt cells.
- untreated - 50% DIE! treated only 1%
- treatment = oral rehydration solutions (glucose and electrolytes)
- Cholera Toxin increases cAMP
- Rehydration??? Na, K, Cl, Citrate + Glucose
Cystic Fibrosis
autosomal recessive disease caused by mutation of chloride transporter (CFTR channel)
- cholera toxin cannot disrupt mutated CFTR channel
- However –> cholera toxin causes irreversible opening of CFTR channel and patients DIE from excessive fluid loss
- SO, cystic fibrosis heterozygotes could be protected from severe cholera
