DIGESTION & ABSORPTION I Flashcards
Mucosa of the small inestine
-
Epithelial layer: single layer of epithelial cells linked by tight junctions
- Endocrine & mucous cells
- Lamina propria: connective tissue containing blood vessels, nerve fibers, and lymphatic ducts
- Muscularis mucosae: thin layer of circular & longitudinal smooth muscle
Submucosa of small inestine
Network of nerves, submucous plexus, blood, and lymphatic vessels
Muscularis Externa of small intestine
Circular layer
Myenteric nerve plexus
Longitudinal layer
Main layers of small intestine
- Mucosa
- epithelial layer
- lamina propria
- muscularis mucosae
- Submucosa - nerves, submucous plexus, blood, vessels
- Muscularis externa
- circular layer
- myenteric nerve plexus
- longitudinal layer
- Serosa
Big structural & functional differences between small and large intestine
-
SI
- Longer
- Has more folds because it has villi
- Absorbs nutrients
-
LI
- Haustra
- K+ secretion
Paneth cells are seen in small or large intestine?
Absorptive cells? Goblet cells? Stem cells? Enteric endocrine cells?
Paneth - Small
Absorptive, Goblet, Stem, and Enteric endocrine - both
Way more absorptive in the small intestine; way more goblet in large
Gut-associated lymphoid tissue (GALT)
Organized aggregates of lymphoid tissue called Peyer patches that sample contents of intestinal lumen via endocytosis and secretes IgA
- protects against pathogens
- provides immunologic tolerance to dietary substances and the good bacteria in the large intestine
- minor: mast cells can release histamine & cytokines
2 systems regulating GI function
Autonomic nervous system - Ach & norepinephrine
Enteric nervous system - sensory, interneurons, motor neurons; only in GI tract
2 methods of regulating GI function
Hormones from enteroendocrine cells (G cells, I cells, S cells) in stomach & SI
Paracrine transmitters released from sensor cells to adjacent cells without entering the blood. Ex) Somatostatin & histamine
Gastrin
Hormone family
Site of secretion
Stimuli for secretion
Actions
Cholecystokinin (CKK)
Hormone family
site of secretion
stimuli
actions
Secretin
Hormone family
Site of secretion
Stimuli for secretion
Actions
“fireman” alkalinizes the acidity
Glucose-dependent insulinotropic peptide (GLIP/GIP)
Hormone family
Site of secretion
Stimuli for secretion
Actions
Describe the structure and function of the components in a villus
Starch
A mixture of straight & branched-chain glucose polymers
- Amylase: straight
- Amylopectin: branched
Glycogen: branched animal starch
What kind of carbs can the SI absorb?
What kind of carbs can the LI absorb?
SI absorbs monosaccharides - nothing larger!
LI doesn’t absorb carbs
Insoluble fibers are carbohydrate polymers that can’ tbe digested and get excreted
Soluble fibers are partially degraded by
enzymes from colonic bacteria
First phase of starch digestion
Luminal digestion of starch by a-amylase
Salivary amylase & *Pancreatic amylase*
- hydrolyze internal a-1,4 bonds in amylose & amylopectin
- CAN’T hydrolyze terminal bonds, a-1,6 bonds (branch points in amylopectin), or a-1,4 bonds immediately adjacent to a-1,6 bonds.
–> result: short oligomers of glucose
- Maltose (dimer)
- Malto triose (trimer)
- a-limit dextrins (from amylopectin)
Second phase of starch digestion
Digestion of oligosaccharides at brushborder
-
Straight-chain oligomers (maltose & maltotriose)
-
Digested by hydrolases:
- glucoamylase
- sucrase
- isomaltase
-
Digested by hydrolases:
- a-limit dextrins
- Digested by isomaltase: cleaves a-1,4 and a-1,6
Result: free glucose monomers
Uptake of glucose & galactose across the enterocyte
-
Sodium/glucose transporter 1 (SGLT1)
- Symporter that takes up glucose (and galactose) against its conc gradient by coupling to Na+
- In the cytosol, glucose & galactose can stay for metabolism or leave across the basolateral GLUT2
Uptake of fructose across enterocytes
Why is it associated with lactose intolerance
- Apical GLUT5 takes in fructose
- Can stay or leave via basolateral GLUT2
Because it’s not coupled to Na+ like glucose & galactose, fructose uptake is inefficient and easily overwhelmed –> lactose-intolerance symptoms
Monosaccarides & disaccarides are completely absorbed in the SI.
The tiny amount of starch that does escape is metabolized by _____ into ____ taken up by ____
Metabolized by colonic bacteria into short chain fatty acids (acetate, proprionate, butyrate) taken up by colonic cells
Lactose intolerance
Lactase deficiency -> undigested lactose goes to the colon, where bacteria metabolize it and release gas that causes dirrhea & discomfort
Sucrase-Isomaltase deficiency
very low levels of sucrase and isomaltase activity in brush border
Glucose-galactose malabsorption syndrome
Mutations in the SGLT1 gene that result in a faulty or unexpressed protein or, more commonly, failure of the protein to traffic appropriately to the apical membrane of enterocytes.
Gastrointestinal symptoms
Oligosaccaridases are normal & fructose is well-tolerated
3 types of enzymes that digest proteins
-
Luminal enzymes from pancreas & stomach
- Peptides -> oligopeptides & aa
-
Brush border enzymes
- Peptides -> oligopeptides & aa
-
Cytosolic enzymes
- Oligopeptides -> aa
Name the luminal enzymes and what activates them
-
Gastric: Pepsinogen -> pepsin 15%)
- Activated by low pH
-
Pancreas: Trypsinogen, chymotrypsinogen, proelastase, procarboxypepidase A & B -> Trypsin, Chymotrypsin, Elastase, Carboxypeptidases
- Activated by trypsin
- Trypsinogen also activated by enteropeptidase (enterokinase from jejunum)
Differentiate between the endopeptidases and the exopeptidases
-
Endopeptidases
- Trypsin, Chymotrypsin, Elastase
- cuts peptide bonds adjacent to specific aa –> oligopeptidases
-
Exopeptidases
- Carboxypeptidases A & B
- cuts peptide bonds adjacent to the carboxyterminus -> aa
- Luminal proteases convert dietary proteins to __.
-
Brush border peptidases then convert those to
- __ (70%)
- Taken across brush border by ___
- __ (about 30%).
- Taken across brush border by ___
- __ (70%)
- In the cytosol of the enterocyte, ___ are cleaved to single ___
- Luminal proteases convert dietary proteins to oligopeptides.
- Brush border peptidases then convert oligopeptides to
-
aa (70%)
- Amino acid transporter
-
dipeptides and tripeptides (30%).
- Small peptide transporter
-
aa (70%)
- In the cytosol of the enterocyte, dipeptides and tripeptides are cleaved to single amino acids
Absorption of oligopeptides
- H+/oligopeptide cotransporter PepT1 (apical)
- Peptidases in the cytoplasm digest oligpeptides -> aa
- Na+/aa transporters (basolateral)
If free glycine is in the lumen, enterocyte absorbs it only via <strong>apical aa transporters; </strong>whereas, glycylglycine in the lumen wil also get absorbed by PepT1
Absorption of aa across luminal membrane
AA enter the enterocyte via Na-dependent (B0,+) and Na-independent (b0,+) transporters on luminal membrane
Peptidomimetic drugs (antibiotics, cancer chemotherapy) are taken up by
PepT1
The movement of aa at the ___ membrane is bidirectional. Explain
basolateral membrane
- aa exit the enterocyte via Na+-independent transporters
- aa enter the enterocyte via Na+-dependent transporters
Villous cells vs Crypt cell
How do they get their necessary aa?
Villous cell (absorptive): amino acid absorbed across the apical membrane are used for protein synthesis in the cell
Crypt cell (secretory):does not absorb amino acids across the luminal side and needs to derive them from the blood across the basolateral membrane
10% of absorbed aa are used for protein synthesis in the ___ cell
villous cell
- _x_ is the major apical transporter for neutral AA.
- It is exploited by another apical transporter, _y__ which brings in _z_ in exchange for neutral AA.
- Then z will exit the basolateral membrane via w .
- If y is defective, then ____ will compensate.
- Na-dependent B0 is the major apical transporter for neutral AA.
- It is exploited by another apical transporter, Na-independent b0,+which brings in dibasic aa & cystine in exchange for neutral AA.
- Then dibasic aa & cystine will exit the basolateral membrane via y+
- If b0,+ is defective, then PepT1 will compensate.
Lysurinic protein intolerance is assocaited with mutations in
basolateral y+L transporter
Hartnup disease
Defective renal & intestinal B transporters –> can’t absorb neutral aa
- Not protein deficient because of normal absorption of oligopeptides
- Suffer from lack of niacin (vitamin B3) which is synthesized from tryptophan, a neutral aa lost in urine.
Cystinuria
Disease caused by a defect in renal & intestinal b0+ transporters.
Accumulation of cysteine in the urine causes kidney stones. No protein deficiency because of normal absorption of oligopeptides.
