• Both active and passive mechanisms participate in GIT absorption
• Both paracellular and transcellular movements are involved
• Absorption area is enlarged by folds, villi and microvilli (mostly in small intestine)
• Absorption of water and electrolytes occurs in both small and large intestine, absorption
of nutrients occurs only in small intestine
• Small intestine absorbs water and electrolytes and secretes HCO3
-, large intestine
absorbs water and electrolytes and secretes potassium and HCO3
•
Water „follows“ electrolytes, eventually is „drafted“ by osmotically active substances
• Numerous absorption mechanisms depend on sodium gradient
WATER BALANCE ( l / DAY )
INTAKE
OUTPUT
saliva
stomach
pancreas
bile
small intestine
colon
2
1,5
2
1,5
0,5
1,5
8,5
0,4
0,1
(7,5)
(1,3)
(0,2)
Diffusion
Facilitated diffusion
Co-transport
Active transport
WATER ABSORPTION
(small intestine, gallbladder, stomach, colon)
(duodenum - osmoticdraft of H2O)
Continuous osmotic gradient
brush border H2O
H2O
FILTRATION
Na+
Na+, K+, Cl-
+10mV
Na+
K+
Cl-
TRANSPORT
•Transcellular
•Paracellular
Brush border
Tight junctions
Basal membrane
Lateral membrane
F
STIMULATION: digestion products (AA, sugars)
TRANSPORT OF ELECTROLYTES
K+
Na+
K+
K+
Na+
Na+
IL
IL
glucose, galactose,
AA
Cl-
H2O+CO2
H+ HCO3
-
H2CO3
H2O + CO2
Gs
cAMP
ClLieberkühn
cryptes: matured cells –
absorption, immature cells – secretion
of Na+, Cl- a H2O
JEJUNUM
ILEUM
choleratoxin (Cl, Na, H2O)
H2O K+
K+
H2O
DIARRHOEA
brush border
basolateral membrane
J
glucose, galactose,
AA
K+
Na+ (120mM/l)
K+
Na+
Na+(25mM/l)+H2O
Cl-
H2O+CO2
H+ HCO3
-
H2CO3
H2O + CO2
TRANSPORT OF ELECTROLYTES
COLON
K+
ClALDOSTERON
ALDOSTERON
ALDOSTERON – synthesis of transport
systems (as in proximal tubule)
basolateral membrane
brush border
K+
REGULATION OF TRANSPORT OF WATER AND
ELECTROLYTES
1. Autonomous nervous system: SYMP (noradrenaline, enkefalins) +
somatostatin – increase of absorption of water, sodium and chlorine
2. Aldosterone: colon – stimulation of secretion of potassium and absorption
of sodium and water (up-regulation of Na/K-ATPase, Na-channel)
3. Glucocorticoids: small intestine and colon - absorption of sodium, chlorine
and water (up-regulation of Na/K-ATPase)
ABSORPTION OF Ca2+
INTAKE: 1000mg/day
ABSORPTION: 350mg/day
Absorption against
concentration gradient (1:10)
in all GIT (D, J), 50x slower
than absorption of Na+
Ca2+
Ca BP
Ca2+-ATPase Na+/Ca2+-antiport
VIT.D
ER
Mch
1,25-dihydrocholecalciferol
Calbindin – prevention of
formation of insoluble salts
(phosphates, oxalates)
[Ca2+]pl.
Basolateral membrane
brush border
TRPV6Ca2+
RACHITIS
(rickets)
ABSORPTION OF Fe2+
endocytosis
2 Fe2+
TRANSFERIN
INTAKE: 15-20mg/day
ABSORPTION:
Men: 0,5 - 1mg/day
Women: 1 – 1,5mg/day
D, J
pH: Fe3+ Fe2+
70% - Hb
25% - F
Insoluble salts and complexes (20:1) – limitation of absorption
Decrease of pH
Fe – up-regulation
Fe2+ stimulates
synthesis of TF – regulation!
Hemosiderin – deposits of Fe in desmosomes
PLAZMATIC TRANSFERIN
(Apo)-Feritin
Excess of Fe2+ – loss with epithelium
Fe2+ stimulates synthesis of
apoferitin (translation) – regulation!
basolateral membrane
brush border
VITAMIN B12
•Daily dose is close to absorption capacity
•Synthesised by bacteria in colon – BUT there is not absorption mechanism
•Store in liver (2-5mg)
•In bile 0,5-5mg / day, reabsorbed
•Daily loss – 0,1% of stores stores will last for 3-6 years
ABSORPTION
1. Gastric phase: B12 is bound to proteins, low pH and pepsin release it; bound to
glycoproteins – R-proteins (saliva, gastric juice), almost pH-undependable; intrinsic
factor (IF) – parietal cells of gastric mucosa; most of vitamin bound to R-proteins
2. Intestinal phase: pancreatic proteases, cleavage of R-B12, bound to IF (resistant to
pancreatic proteases)
ABSORPTION OF B12 VITAMIN
IF B12
B12
B12
IF
IF
Intrinsic Factor
IF-B12
receptor
complex
?
B12
B12 B12
v.portae
TERMINAL
ILEUM
B12
transcobalamin II
Pernicious anaemia
(megaloblastic)
DIGESTION AND ABSORPTION OF SACCHARIDES
POLYSACHARIDES
(a-glycosyled s.)
OLIGOSACCHARIDES
MONOSACHARIDESFRUCTOSE GLUCOSE GALACTOSE
AMYLOPECTIN
GLYCOGENa-amylase
DEXTRIN
TRICHACHARIDES
DISACHARIDES: SACCHAROSE MALTOSE LACTOSE
Isomaltase
Maltase
Saccharase
Lactase
Saliva
Pancreatic juice
Na+
Epithelium of duodenum and jejunum
•Lactase intolerance
•Diarrhoea
salivary amylase
2 binding sites for Na+
1 binding site for saccharide
facilitated transport + diffusion
GLUT-5 SGLT-1
GLUT-2
DIGESTION AND ABSORPTION OF PROTEINS
STOMACH
Pepsin
DUODENUM
Trypsin
Chymotrypsin
Carboxypeptidase
JEJUNUM
Membrane peptidases
(brush border)
CYTOPLASMA of epithelial cell
di-, tri-peptidases
PEPTIDES > 4 AA
DI-, TRI-PEPTIDES
AA
AA
PROTEASES
15%
50%
PEPTIDASES (exo-, endo-)
NUCLEASES
Na-cotransport Diffusion
Purine, pyrimidine bases
– active transport
100g food + 30g GIT juices + epithelial cells
enterokinase
ABSORPTION OF
LIPIDS
Triglycerides (TAG)
Sterols (-esters)
Phospholipids (lecithin)
LIPID DROPS
EMULSIFICATION (+lecithin, +monoglycides)
Ø 1mm
BILE ACIDS SALTS
DEESTHERIFICATION
PANCREATIC LIPASE (colipase)
CHOLESTEROL-ESTHERASE
PHOSPHOLIPASE A2
ENTERIC LIPASE
Glycerol FA MAG CH LFL
MICELLES
Ø 5nm, 20-30
molecules
polar stratification, hydrophilic
disintegration of micelles
TAG
unstirred water layer
200-500mm
bile acids
resorption (diffusion)
reesterification (FA >12c, in endopl.retic.
CHE PL
PROT.
EXOCYTOSIS
CHYLOMICRA Ø 10nm
LYMPHATIC CIRCULATION
NEFA (<12c)
GLYCEROL
capillaries (fenestration)
Na+
DIGESTION AND ABSORPTION OFDIGESTION AND ABSORPTION OF
ABSORPTION IN COLON
• Na+ (active, aldosteron) H2O (90% water in colon)
• Cl•
Vit. K, B
• AA, lactate, bile acids, FA
REST OF CHYME
1. Cellulose, collagen
2. Bile acids, epithelia, mucin, leucocytes
• Bacteria fermenting: fibre (pectin, cellulose) – lactate, alcohol, acetate, CO2, methane
• Bacteria putrescent: residues of AA – NH3, SH2, phenol, indole, solatol (carcinogenic)
Production of vitamin K and vitamins of B group
NUTRITION
PASSAGE EUMICROBIA