05b: Intestinal Absorption Flashcards
T/F: Absorption of CHO, proteins, and fats is complete in upper half of small intestine.
True
The distal 1/3 of intestine is essential for absorption of:
Vit B12-IF complex and bile salts
T/F: Most water, vit/minerals absorbed in distal half of small intestine.
False - proximal half
Tight junctions throughout intestine exhibit variable permeability to (X) compounds. Where along intestine are these junctions more/less leaky?
X = water and ions;
More leaky at proximal small intestine and grow tighter gradually toward colon
The transepithelial potential difference in intestine/colon is positive on (luminal/ISF) side. Would you expect this difference to be greater in small intestine or colon?
ISF;
Colon (less permeable tight junctions)
Brunner’s glands in (X) part of GI tract secrete (acidic/neutral/alkaline) and (serous/mucous) fluid that likely serves (Y) function.
X = duodenum (submucosa)
Alkaline
Mucous
Y = protective
Most CHO we consume is in the form of (mono/di/poly)-saccharides. Which of these forms of CHO can be absorbed in small intestine?
Polysaccharides/starch (60%);
Only monosaccharides!
The enzymes that can breakdown poly/di-saccharides into monosaccharides come from/reside in (X). List some of these enzymes.
X = anchored in luminal membrane of enterocytes;
- Maltase and isomaltase
- Lactase
- Sucrase
T/F: Enzymes on enterocytes that break down CHO to monosaccharides all have specific substrates.
False - some hydrolyze more than one substrate
T/F: Lactase can only hydrolyze lactose.
True
T/F: Sucrase can only hydrolyze sucrose.
False - but sucrose can only be hydrolyzed by sucrase
Following normal meal, most ingested CHO is digested/absorbed in (first/middle/last) (X)% of small intestine.
First;
X = 20
Which monosaccharides share common mechanism of transport into enterocytes? Which mechanism is that?
Glucose and galactose;
Na-dependent co-transport (via SGLT1 carrier)
T/F: Glucose, galactose, and fructose compete for the same apical carrier in small intestine.
False - only glucose and galactose do
Apical uptake of fructose in small intestine is via (X) (carrier/channel) and is dependent on (ATP/Na).
X = GLUT5 carrier
Neither
Intestinal absorption: Basolateral exit of (X) monosaccharides is (up/down)-hill via (Y) (transporter/channel).
X = glucose, galactose, fructose
Downhill
Y = GLUT2 (facilitated transporter)
Some evidence shows that tight junction permeability (increases/decreases) following activation of SGLT1 transport, which is responsible for (X). What’s the function of this?
Increases;
X = apical transport of glucose and galactose
Allows paracellular absorption of glucose if its luminal concentration is high
In glucose-galactose malabsorption syndrome, (X) transport system is not functioning. What’s fed to infants with this disorder?
X = SGLT1 (Na-dependent, brush border sugar transport system);
Fructose
Oral sugar tolerance test: if patient is intolerance, (X) symptom will ensue and sugar will appear in (blood/feces).
X = diarrhea
Feces
T/F: Most protein absorption takes place in ileum.
False - nearly completely absorbed by the time it’s traversed the jejunum
T/F: Intact proteins and large peptides cannot be absorbed in intestine.
False - only in minute amounts via receptor-mediated endocytosis
T/F: Any protein leaving the stomach is in the form of peptides since no enzyme can break them down to AA.
False - pepsin can reduce small amount into AA/peptides
T/F: Small peptides are significantly more concentrated than single AAs in intestinal lumen.
True (about 3-4x)
T/F: The rate of AAs exceeds the rate of di-peptides/tri-peptides.
False - vice versa
AA transporters in small intestine are classified according to which characteristics?
- Specificity for groups of AA (neutral, acidic, etc)
2. Na- dependent/independent
PepT1 is a(n) (X)-dependent transport system for (Y).
X = proton Y = small (di/tri)-peptides
In addition to the transporters, diffusion across (apical/basolateral) membrane is possible for small, (X) AAs.
Basolateral;
X = hydrophobic
Hereditary disorders involving malfunctioning AA transporters are likely recognized by (presence/absence) of AAs in (blood/urine/feces). Why?
Presence;
Urine;
AA transporters defective in enterocytes also found (and defective) in renal tubule
T/F: In AA absorption defects, malnutrition does not ensue since AAs can be absorbed in di/tri-peptide form.
True
With daily ingestion of (X) volume water and GI secretion of (Y) volume fluid, how much fluid does intestine absorb each day?
X = 2L Y = 7L
9 L absorbed
List the key locations in GI tract where significant water reabsorption takes place.
Jejunum and (to lesser extent) ileum
Intestinal water absorption is secondary to (X) (secretion/reabsorption). This phenomenon is referred to as (Y).
X = Na reabsorption Y = standing osmotic gradient
T/F: Water absorption in GI tract takes place only minimally through aquaporins and moreso through tight junctions.
False - NO aquaporins found as of yet
List the location in GI tract where Na reabsorption rate is highest. Where along tract does Na absorption not occur?
Jejunum;
Na absorbed along the entire length of intestine
Na transport across (luminal/basolateral) membrane requires Na/K ATPase in (X) part of intestine. Why is the ATPase needed?
Basolateral;
X = all
Na exiting is against its electrochemical potential difference (ISF is more positive than lumen)
ENaC, aka (X), is (transporter/channel/ATPase) found in (apical/basolateral) membrane of (Y) part of GI tract. It’s responsible for:
X = epithelial Na channel
Apical;
Y = colon
Na absorption into colonic cells
Na transport in colon, via (X) mechanism, is stimulated by (Y) hormone/NT.
X = ENaC (channel) Y = aldosterone
Any left-over HCO3 in intestinal lumen is reabsorbed in (X) location and involves the (secretion/absorption) of (Y).
X = jejunum
Secretion;
Y = H+ (to form CO2 that diffuses across membrane)
T/F: During intestinal reabsorption of HCO3, the molecule absorbed from lumen is technically a different one than that secreted into blood.
True - enters cell as CO2 and then carbonic anhydrase does its thing within cell to form H and (new) HCO3
T/F: From jejunum onward, HCO3 is only up for reabsorption.
False - colon normally secretes HCO3 in exchange for Cl
Colon (secretes/absorbs) HCO3 via (trans/para)-cellular mechanism.
Secretes;
Transcellular (HCO3/Cl exchange)
Large paracellular absorption of Cl occurs in (X) part of GI tract. It’s driven by:
X = jejunum
Electrical potential difference (set up by Na absorption)
Feces is typically (neutral/alkaline/acidic) and has relatively high concentration of (X) ion.
Alkaline;
X = K
In small intestine, K is usually (absorbed/secreted). What’s the mechanism and driving force?
Absorbed (lumen to blood);
Paracellular diffusion; lots of water reabsorbed raises K conc in lumen
In the colon, K is normally (absorbed/secreted) in (para/trans)-cellular manner.
Secreted;
Both
In disease like cholera, the toxin (activates/inhibits) (X), leading to increased intestinal (absorption/secretion) and (Y) symptom.
Activates; X = AC (irreversibly) Massive secretion (of electrolytes and water); Y = diarrhea
Mechanism for Ca absorption in intestine depends on level of (X). What are the two potential mechanisms?
X = intake;
- Paracellular (ileum; adequate intake)
- Transcellular (duodenum; low intake)
Transcellular absorption of Ca: entry into cell is (uphill/downhill) via (X) (channel/transporter/ATPase).
Downhill;
X = Ca channel (TRPV 6)
T/F: Ca absorption in small intestine depends on voltage-sensitive Ca channel (TRPV 6).
False - it’s voltage-insensitive
Transcellular absorption of Ca: which step is rate-limiting? This step requires (X).
Intracellular diffusion;
X = calbindin (Ca-binding protein)
Transcellular absorption of Ca: exit from basolateral membrane involves (X) (channel/transporter/ATPase).
X = Ca ATPase and Na/Ca exchange
How does Vitamin D play role in enhancing (X) mineral (absorption/secretion)?
X = Ca absorption;
Increase synthesis of calbindin and Ca ATPase
(X) absorption is tightly regulated because it can have deleterious effects. Further, it’s sequestered by proteins: (Y) in plasma and (Z) in cells.
X = Fe Y = transferrin Z = ferritin
Most Fe absorption takes place in (X) portion of GI tract, where (Y) enzyme on surface of cells makes it more soluble by:
X = upper duodenum Y = ferrireductase (on brush border)
Reducing Fe3+ to Fe2+ (more soluble)
Fe absorption: Free (ferrous/ferric) ion crosses apical membrane via (X).
Ferrous;
X = Divalent Metal Transporter (DMT1)
Fe absorption: some (ferrous/ferric) ions can be absorbed while bound to (X). How are they freed intracellularly?
Ferrous;
X = heme
Heme oxygenase frees ion
Fe that is lost in the feces is (free/bound). Elaborate.
Bound to ferritin;
This binding occurs in enterocytes and is near irreversible
Calbindin is to Ca what (X) is to Fe.
X = mobilferrin
Fe absorption: upon exit through basolateral membrane via (X), Fe undergoes which changes for transport into blood?
X = ferroportin
Oxidized to ferric ion (via ferroxidase) and incorporated into plasma transferrin
Apoferritin, produced by (X) cells, (increases/decreases) when Fe stores are abundant.
X = mucosal
Increases (binds more Fe so more Fe lost in feces)
(X) is a peptide released by liver that (increases/decreases) Fe absorption via which mechanism?
X = hepcidin
Decreases;
Initiates internalization/degradation of basolat ferroportin transporter
List the three main mechanisms that regulate Fe absorption.
- Apoferritin levels
- Hepcidin
- Hypoxia inducible transcription factor
