Digestion/Absorption Flashcards
Drug inhibiting lipase
Olestra
fat soluble vitamins
A, E, D,K
water soluble vitamins
biotin, folic acid (simple diffusion), vitamin B12 (specific transporter)
channel critical for absorption
Na/K ATPase pump
water absorption linked to what?
Na absorption
channels for Na absorption
Na/glucose & galactose or Na/amino acid cotransport, NaCl cotransport, Na/H exchange, passive diffusion
Chloride absorption
passive in proximal intestines, more in distal ileum/colon due to less leaky TJs; Cl exchanged for HCO3 of setting acids from bacteria
K absorption: active or passive?
passive
Potassium absorption
paracellular movement in jejunum; transcellular incolon
Ca absorption
Ca and Mg compete for uptake
- Ca enters enterocyte passively down electrochemical gradient in proximal intestines-Ca ATPase pumps Ca out into blood
Vitamin D
synthesized in skin/absorbed by intestine
where is vitamin D is vitamin D metabolism
- vitamin D is 25-hydroxylated in liver
- 25-OH Vit D is 1-hydroxylated in kidney in presence of parathyroid hormone
- Vit D binds to cytoplasmic receptor, activating transcription/translation
how does vitamin D relate to Ca
vitamin D stimulates uptake of Ca by increasing Ca binding proteins and Ca ATPase molecules
Where is iron absorbed?
regulated absorption in proximal intestines
fates of Fe
-transported across apical membrane as heme or Fe (receptor mediated)
THEN
- binds to apoferritin to form ferritin – stays in cell and lost when cell dies
OR
- binds to transferrin (carrier protein), leaves the cell adn goes into blood
trend of water permeability through intestines
paracellular water permeability decreases from proximal to distal in the small intestines
- lowest in colon since trying to solidify waste and needs to link water movement to transcellular ion movement
Osmotic diarrhea causes
(due to impaired digestions/defects in absorption)
- lactase deficiency
- ileal resection – bile salts not absorbed
- Celiac disease
Celiac disease
- Sprue; genetic
- with gluten sensitivity –> gliaden-induced destruction of villi
Vibrio cholerae causes what kind of diarrhea
Secretory diarrhea– increases cAMP levels in cells and in turn activates CF chloride channel (and thus water) on the luminal surface
- also have paracellular movement of Na into lumen and thus water as well
Oral rehydration therapy
antibiotics plus KHCO3 to prevent hypokalemia and metabolic acidosis, glucose (or amino acids) with NaCl to facilitate absorption of electrolytes and water
biggest risk factor for dehydration
hypokalemia
Amylase
secreted by salivary glands into mouth/stomach; digests starch to create polysaccharides
- also secreted by pancras into duodenum/jejunum to digest starch into polysaccharides
lingual lipase
secreted by serous glands of tongue
- digests fat into monoglycerides and fatty acids
- present in mouth ant stomach
pepsin
- secreted by stomach
- digests proteins into polypeptides
Trypsn
secreted by pancreas into duodenum/jejunum to breakdown protein/polypeptides into small peptides and amino acids
chymortypsin
secreted by pancreas into duodenum/jejunum to break down proteins/polypeptides into small peptides and amino acids
elastase
secreted by pancreas into duodenum/jejunum to break down proteins/polypeptides into small peptides and amino acids
carboxypeptidases
secreted by pancreas into duodenum/jejunum to break down proteins/polypeptides into small peptides and amino acids
lipase and colipase
secreted by pancreas into duodenum/jejunum to digest fat into monoclycerides, fatty acids, and cholesterol
Phospholiase A2
secreted by pancreas into duodenum/jejunum to digest fat into monoclycerides, fatty acids, and cholesterol
Cholesterol ester hydrolase (non-specific lipase)
secreted by pancreas into duodenum/jejunum to digest fat into monoclycerides, fatty acids, and cholesterol
Bile salts
secreted by liver into duodenum/jejunum to emulsify and dissolve fats
HCL
secreted by stomach to kill bacteria and denature proteins
NaHCO3
ubiquitous; buffers pH
Mucus
ubiquitous; lubrication, protection of mucosal surfaces
pepsinogen
zymogen released by chief cells into stomach; converted to active pepsin by stomach acid
typsinogen
secreted into duodenum and activated to trypsin by enterokinase
largest source of starch in most human diets
amylopectin (plant starch) containing alpha 1,4, and alpha 1,6 linkages
cellulose
polymer linked by beta 1,4 linkage that can’t be digested by intestinal enzymes; major component of dietary fiber
amylase digestion
catalyzes internal alpha 1,4, bonds to generate maltose, and maltotriose and alpha-limit dextrin
- never glucose as product
2 types of glucose polymers in diet
amylose, amylopectin
role o fenzymes in brush border
convert small polysaccharides to sugar monomers
surase-isomaltase (SI)
breaks down 1,6 linkages of alpha-limit dextrin to glucose
maltase-glucoamylase (MGA)
breaks down maltriose to glucose
lactase
breaks down lactose to glucose
sucrase
breaks down sucrose to glucose
how to transport sugars into cells
intestinal sugar transporters
- Na-dependent glucose transport (SGLT1)
- Na-independent fructose transporter (GLUT5; GLUT2)
Na - dependent glucose transporter
(SGLT1)located on apical side of enterocytes and transports glucose, galactose, and Na from intestinal lumen to cytosol
Na-independentfructose transporter
(GLUT5 and GLUT2)
- GLUT5 = apical; transports fructose form luemnt to cytosol
- GLUT2 basolateral and transports all 3 monosaccharides (fructose, glucose, galactose) from cytosol to blood
lactose intolerance
- lactase absent from brush border
- unabsorbed lactose draws water into intestinal lumen – osmotic diarrhea
- gut bacteria metabolize lactose to form gases
Absent SGLT1
Na/Glucose cotransporter; absence auses malabsorption fo glucose/galactose
- diarrhea when ingesting dietary sugars due to reduced SI absorption fo Na and fluid; also fluid secretion due to osmotic effects of non-absorbed monosaccharide
- potentially fatal neonatal condition of glucose-galactose malabsorption
treat absent SGLT1 transporter
replace dietary glucose with frucose
where is protein digestion
begins in stomach with pepsin; completed in SI with gastric, pancreatic, enterocyte brush-border and cytoplasmic peptidases
2 classes of peptidases
endopeptidases and exopeptidases
role of secreted endopeptidases
hydrolyze interior peptide bonds
examples of endopeptidases
Pepsin (aromatic aa)
Trypsin - arginine/lysine
Chymotrypsin (aromatic aa)
Elastase (neutral aliphatic aa)
secreted exopeptidase role/examples
- hydrolyze one amino acid at a time from C-terminus of proteins/peptides
- Carboxypeptidases A
- Carboxypeptidases B
brushborder proteases
- aminopaptidase
- Dipaptidyl aminopeptidasel
- dipeptidase
aminopeptidase
exoprotease at brush border removes one aa from N terminus at a time
dipeptidyl aminopeptidase- removes
brush border enzyme; removes dipeptides from N terminus
dipeptidase
brush border enzyme; converts dipeptides to amino acids
amino acid absorption in intestine
via H dependent peptide transporter PEPT1
fatty acid absorption
short chain fatty acidsdiffuse across apical memrane and re-esterified as triglycerides in smooth ER prior to uptake into chylomicrons that exocytose acros BL membrane
when is pepsin active
below pH 5
SI proteases
trypsinogen, chymotrypsinogen, pro-elastase, pro-carboxypeptidase A, pro-carboxypeptidase B
Steps of Si protein digestion
- Trypsinogen activated at brush border by enterokinase
- trypsin activates all other precursors
- trypsin, chymotrypsin, elastase, carboxypeptidase A and B hydrolyze protein to aa and di-tri- and oligopeptides
- brush border proteases hydrolyze oligopeptides to amino acids
- pancreatic proteases digest themselves and each other
Protein absorption
by Na-dependent co-transport; di- and tripeptides absorbed (compared to only carbohydrate monomers)
- up to 70% protein absorbed this way
specificities of 4 different amino acid carriers
neutral, basic, acidic, epcial one for proline/glycine
what happens to protein inside enterocytes
di- and tripeptides hydrolyzed to amino acids by cytoplasmic proteins and exit BL membrane by facilitated diffusion to enter blood capillaries
cysteinuria
genetic absence/defect of Na-amino acid transporters; same Na-amino acid transporter missing in kidneys
- lack capacity for renal or intestinal absorption of cystine, lysine, arginine, and ornithine amino acids, so many excreted
- renal defect – excreted amino acids in urine
Hartnup disease
genetic absence/defect of neutral amino acid transporter
Cystic fibrosis
genetic absence/defect of Cl channel called CFTR
4 mechanisms of protein uptake
- Active transport with Na (amino acids)
- secondary active transport with Na (amino acids)
- Secondary active transport with H (di/tripeptides)
- Diffusion across basolateral side
steps in triglyceride digestion
- Fat droplets emulsified by bile salts and lecithin to form small particles and increase surface area for digestion
- lipase and colipase digest triglycerides into 2-monoglyceride and 2 fatty acids that are then solubilized into bile-salt micelles to move to brush border –
- monoglycerides and fatty acids dissociate and passively absorbed at brush border
micelle
- cylindrical structure with hydrophobic groups oriented interiorally and hydrophylic groups oriented towards aqueous phase
- needed to transport products of fat digestion through water layer near surface of enterocytes
What happens to fats after crossing apical membrane
- monoglycerides and fatty acids cross apical membrane by passive diffusion
- put into chylomicrons that travel to Golgi where they are incorporated into secretory vesicles
- secretory vesicles travel to basolateral membrane where contents extruded into interstitial space and taken up into lacteals
Fat malabsorption-associated disorders
Liver disease (can’t make micelles due to bile salt deficiency)
Pancreatic insufficiency (and CF) -lack enzymes to digest fat
weight loss meds - -inhibit lipase
