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43 Cards in this Set

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Carbohydrate Digestion
Must be digested into monosaccharides before being absorbed
Carbohydrate Digestion: Starches
1) Converted by salivary and pancreatic α-amylases to: A) Maltose B) Maltotriose C) α-limit dextrins 2) Oligosaccharides then hydrolyzed to glucose by: A) Glucoamylase B) Isomaltase C) Maltase in brush border membrane
Carbohydrate Digestion: Sucrose
cleaved by sucrase in brush border membrane to glucose and fructose
Carbohydrate Digestion: Lactose
cleaved by lactase in brush border membrane to glucose and galactose
Carbohydrate Digestion: Trehalose
cleaved by trehalase in brush border membrane to
glucose
Carbohydrate Digestion: Cellulose
Not digested by human enzymes
Carbohydrate Absorption
1. intestine will only absorb monosaccharides – glucose, galactose, and fructose 2. glucose and galactose absorbed into enterocyte by common Na+-dependent
active transport system 3. because (Na+, K+) ATPase keeps intracellular [Na+] low, Na+ transported
down gradient; thus energy favorable for transport of glucose/galactose 4. almost all glucose and galactose present in intestine absorbed 5. subsequently transported from cell to blood by facilitated diffusion 6. fructose absorbed exclusively by facilitated diffusion; cannot be absorbed
against concentration gradient
Lactose Intolerance
1) Caused by deficiency in lactase 2) Lactose remains in GI tract as unabsorbed solute, thus decreasing absorption of water by intestine and leading to diarrhea 3) Undigested lactose metabolized by colonic bacteria 4) Symptoms: A) Intestinal distension B) Borborygmi (gurgling noises in intestines) C) Gas D) Diarrhea
Protein Sources
1) Endogenous 2) Exogenous
Protein Sources: Endogenous
Secretory proteins and cells shed into GI tract lumen
Protein Sources: Exogenous
Dietary proteins
Protein Digestion: Overview
1) Proteins absorbed as: A) Amino acids B) Dipeptides C) Tripeptides 2) Larger peptides poorly absorbed, if at all 3) Essentially all ingested protein assimilated
Endopeptidase Types
1) Gastric pepsin 2) Pancreatic enzymes
Exopeptidase Types
Carboxypeptidases A and B
Endopeptidase Function
Hydrolyze interior peptide bonds
Exopeptidase Function
Hydrolyze one amino acid at a time 2) C terminus to N
Gastric Pepsin
Digest small amount of ingested protein
Pancreatic Enzymes
Secreted as inactive precursor: 1) Trypsinogen 2) Chymotrypsinogen 3) Proelastase
Trypsinogen
Converted to active trypsin by enterokinase
Enterokinase
Converts trypsinogen to active trypsin
Trypsin
Autocatalyzes conversion of 1) Trypsinogen to trypsin 2) Chymotrypsinogen to chymotrypsin 3) Proelastase to elastase
Carboxypeptidases A and B
1) Exopeptidases 2) Hydrolyze one amino acid at a time (C-N terminus) 3) Secreted from pancreas as proenzymes 4) Converted to active enzymes by trypsin
Peptidases in Brush Border Function
Cleave peptides produced by pancreatic proteases
to oligopeptides and amino acids
Protein Absorption
1. most amino acids absorbed into enterocytes by Na+-dependent co-transport 2. separate transporters for neutral, acidic, basic, and imino amino acids 3. transported into blood by facilitated diffusion 4. transport of di- and tri-peptides faster and more efficient than for amino acids; uses H+-dependent co-transporter peptide transporter 1 (PEPT1)
5. following meal, majority protein absorbed in form of di- and tri-peptides; most absorbed peptides then hydrolyzed to amino acids by cytoplasmic peptidases in enterocytes 6. protein in stools from bacteria and cellular debris 7. whole proteins can be absorbed, but insignificant nutritionally; more
important immunologically, as this can lead to food allergies
Protein Assimilation Abnormalities
1) Congenital lack of trypsin or pancreatic disease causing trypsin deficiency 2) Congenital defects in transport of amino acids in gut and kidney
Congenital Defects in Transport of Amino Acids in Gut and Kidney
1) Cystinuria 2) Hartnup disease 3) Prolinuria
Cystinuria
Affects uptake of basic amino acids
Hartnup Disease
Affects uptake of neutral amino acids
Prolinuria
Affects reabsorption of proline
Iron Absorption
1) Small fraction of iron (~10%) ingested each day absorbed; amount absorbed about equal to what is lost 2) Absorbed as heme (bound to hemoglobin or myoglobin from meat) or as free iron
Heme Iron
1) Porphyrin moiety containing bound iron 2) Most easily absorbed form of iron 3) Taken up by enterocyte either by receptor-mediated endocytosis or by transporter protein (HCP1) 4) Heme then broken down by heme oxygenase to release free iron
Dietary Free Iron Digestion
1) Two forms of dietary free iron: A) Ferrous (Fe2+) iron absorbed more readily B) Ferric (Fe3+) iron insoluble and can precipitate; most dietary iron is ferric 2) Gastric acid dissolves iron and permits it to form soluble complexes with
ascorbic acid 3) Ascorbic acid (vitamin C) and citric acid promote absorption by forming soluble complexes with iron and reducing ferric iron to ferrous iron 4) Brush border enzyme Dcytb (Duodenal cytochrome b) reduces ferric to ferrous iron
5) Ferrous iron transported across brush border membrane into enterocyte by ferrous iron transporter DMT1
6) Free or ionized iron cytotoxic, so iron in cell binds very tightly to apoferritin protein to form ferritin for storage 7) Absorbed iron transported to basolateral membrane 8) If necessary, transported out of enterocyte into plasma by ferroportin 9) Ferroportin and ferroxidase hephaestin convert ferrous to ferric iron 10) Ferric iron can now bind to plasma transferrin to be transported to other tissues
Iron Digestion Regulation
1. body has no mechanism for removing excess iron, so absorption is regulated 2. amount of iron entering the body and released from storage sites tightly
regulated according to body iron requirements 3. much of this regulation orchestrated by liver-derived peptide hepcidin 4. hepcidin regulates entry of iron into plasma by binding directly to ferroportin 5. this leads to internalization and degradation of ferroportin, which blocks
cellular iron export and reduces plasma iron
Low Iron Levels and Hepcidin
1) Hepcidin levels are low 2) Leads to: A) Increased iron absorption B) Elevated iron release from enterocytes
High Iron Levels and Hepcidin
1) Liver secretes more hepcidin 2) Decreases export of iron from enterocytes 3) Enterocytes containing ferritin-bound iron lost into intestine
Disorders of Iron Absorption
1) Iron deficiency 2) Hemochromatosis
Iron Deficiency
Most prevalent nutrient deficiency and most common cause of anemia in world
Hemochromatosis
1) Chronic absorption of too much iron 2) Hereditary hemochromatosis most common genetic disorder in US 3) Defect in HFE gene causes hepcidin levels to drop through mechanism that is
unknown 4) Excess iron collects in liver, which can lead to cirrhosis and eventually liver cancer 5) Can also damage pancreas, leading to diabetes 6) Contributes to coronary disease 7) Treated by periodically removing blood
Small Intestine Absorption of Water and Electrolytes: Sources
1) Not only dietary H2O and Na+ but also H2O and Na+ contained in salivary, gastric, biliary, and pancreatic secretions 2) Failure to do so leads to: A) Rapid dehydration B) Electrolyte imbalance C) Circulatory collapse
Small Intestine Absorption of Water and Electrolytes: Routes
1) Transcellular 2) Paracellular
Na+ Transport
1. Na+ moved from lumen of small intestine across apical membranes of
enterocytes by four mechanisms a. restricted diffusion through channels b. Na+-glucose or Na+-amino acid co-transport c. Na+ - Cl- co-transport d. Na+ - H+ exchange
2. mechanisms vary over length of small intestine a. in duodenum and jejunum, Na+ absorbed mostly by Na+-glucose or Na+-
amino acid co-transport and Na+- H+ exchange b. in ileum Na+ also absorbed by co-transport with Cl- c. in colon Na+ absorbed through channels
3. Na+ extruded from enterocyte across basolateral membrane by (Na+ - K+) pump; keeps intracellular Na+ levels lower than in lumen, thus promoting transport of Na+ into cell
Cl- Transport
1) Passive diffusion via paracellular route down electrochemical gradient established by transport of Na+ 2) Co-transport with Na+ and K+ 3) Exchange with HCO3-
Water Absorption
1. secondary to and dependent upon solute absorption 2. active reabsorption of electrolytes and nutrients creates osmotic gradient
favoring passive reabsorption of H2O