HECKdigestion of lipids and vitamins Flashcards
absorptive cells are generally found where? what bout secretory
absorptive on surface on villi
secretive in crypts
what type of cells are in the colonic crypts
gland cells
majority of dietary lipids are what
triacylglycerols TAGs
what is the rest of the dietary lipids
phosphlipids from cell membranes and cholesterol (unesterified)
where is esterified cholesterol found
liver and blood foods
What lipids are found in bile
phsopholipids (lecithin) and unesterified cholesterol
what is the first process of digesting dietary lipids
emulsification (chewing, gastric churning, peristalsis, movement between pylorus and duodenum)
forming oil droplets in aqueous solution
As we emulsify food how does SA change
SA on the droplets increase as they get smaller
describe structure of oil droplets
monolayer at interface formed by dietary and secreted lipids. core of triglycerides, diacylglycerol
What is the process of digestion
lypolysis
what enzymes are part of lypolysis
lipases to hydrolyze lipids
describe gastric lipase
active at pH 4
resistant to Pepsin
inactivated by pancreatic proteases in bile salts in the SI
What happens to gastric lipase in someone with an pancreatic deficiency
extended activity of gastric lipase in duodenum
What is the action of gastric lipase
cleaves FA from TAGs
leaves one protanated FFA and one diacylglycerol
Describe pancreatic lipase
major lypolytic enzyme from pancreas
secreted into duodenum in huge excess
what is the secretion of pancreatic lipase dependent on
Colipase alkaline pH of SI Ca bile salts Fatty acid substrate
What is the action of pancreatic lipase
at oil-water interface colipase is necessary to reduce inhibition from phospholipids or proteins on micelle surface
hydrolyze all TAGs resulting in 2 FFA and 1 monoacylglyerol
most dietary lipids are digested as what
triglycerides
What must triglycerides be degraded into before taken up
FFA and Monoacylglycerides
Why did Alli drug cause oily stool
inhibits pancreatic lipase, prevents breakdown into FFA and MAGs from TAGs
What is Phospholipase A2
pancreatic enzyme
needs bile salts and alkaline pH in SI
What is the action of phospholipase A2
cleaves FFA from glycerophospholipid (at SN2 position)
leaves lysophospholipd, no middle fatty acid
Where is phsopholipase A2 found
SI and large intestine from all bacteria
Describe Carboxylester hydrolase
not substrate specific, hydrolyzes all esters, releases free cholesterol and glycerol
What is the action of carboxyl ester hydrolase
equivalent to bile-salt stimulated milk lipase
what is the role of bile salt stimulated milk lipase
lipase in the milk that aids in digestion since pancreas is not yet functioning.
Not activated until reaches duodenum with basic pH
What is the action of bile salt stim milk lipase and carboxyl ester hydrolase
hydrolyzes DAGs, MAGs, TAGs
What stimulates CCK
release of FFA in duodenum
What is the action of CCK
stimulates bile flow in duodenum and secretion of pancreatic enzymes (lipase and esterase)
What does it mean with there are lipids in stools
intact acylglycerols rarely found even in severe malabsorption
What is the test for stool fat
Sudan III staining, a dye that shows presence of oil droplets
Why is there no fat generally found in stool
bacteria like to digest in colon
Where are med chain FA absorbed
independent of micells or bile salts
can diffuse towards enterocytes- directly transferred to blood
What can be used as FA subsititue for patients with malabsoprtion
medium chain fatty acids
The larger acylglycerides are in what part of emulsion droplet
core
smaller on outside
Describe an emulsion droplet with multi layers
multilamellar at the begining but during digestion the layers decrease until it is a micelle
What is a micelle
lipid monolaryer with tails facing hydrophobic core
bigger SA with shorter distance for substrates to cross
What is a unilamellar droplet
one lipid bilayer around droplet
What are the surface components of a micelle
cholesterol, MAGs, lecithin’s(phosphotidylcholine), pancreatic lipases, bile salts, liquid crystalline layer of bile salts and surface components and Ca rich FA soaps
What are in the core of micelles
DAGs, TAGs and cholesterol esters
What happens when MAGs are hydrolyzed on surface by lipases
FFA released
What replace the MAGs when hydrolyzed by lipases
replaced by DAGs and TAGs (originate from core
Increased deposition of liquid crystalline layer of micelle causes what
budding of multilamellar vesicles from emulsion droplet
Bile salts convert multilamellar vesicle to what
unilamellar
do bile salts hinder or assit micelle formation
assist
micelles have to cross what area to enter
the mucous layer
What are the microclimates of the intestine that micelles cross
bulk water area(hydrolysis and micelle formation)
mucus gel layer (barrier for bacteria)
unstirred water layer (juxtaposed to cell membranes)
What does the unstirred water layer allow
diffusion of short and medium chain FA monomers into enterocytes
larger chains must be formed into micelles
What liberates the FA from micelles into enterocytes
protonated environment
Do micelles diffuse across lipid membranes
no, the lipids leave and cross
What maintains the H [ ] in the unstirred water layer
Na/H exchanger
What allow lipids to cross lipid bilayer
diffusion
FA translocases and FA binding proteins to enhance translocation
What happens to lipids in the enterocyte
re-esterification
long chain FA are assembled back into TAGs and phopholipids in the sER
rER to package into lipoprotein particles (apolipoproteins trafficked to sER and golgi)
What occurs in the sER of enterocytes
apolipoprpteins meat TAGs, phospholipids and choesterol esters form chylomicrons (covered in lecithin and phospholipids) and form VLDLs (carry endogenous lipids during both fed and fasting states)
Where are lipoprotein particles trafficked
to golgi from sER
apolipoprotein A1 associates and glycoslyation occurs, vesicles carry chylomicrons and VLDLs from golgi trans to the basolaterl membrane and fuse to release contents
Why do chylomicrons and VLDLs have to enetr lymph and not blood
too big to enter fenestrated capillaries, have to go thru cisterna chyli and thoracic duct to enter circualtion via subclavian v
Where are water soluble vit absorbed and desribe characteristics
absorbed in SI
have specific carriers and or brush border and luminal enzymes for deconjugatoin and phosphorylation
many Na dependent
many utilize GPCR and cAMP
Describe Fat soluble Vit
chemical structure is hydrophobic(dissolved in fat deposits not aquesous environment)
rely on lipid absorption because chemical structure
What hapens to fat soluble Vit in enterocyte
diffuse to sER (specific carriers (retinol binding is for Vit A))
associate with lipid to form chylomicrons and VLDLs (same path then)
What can cause fat soluble vit deficiency from malabsorption
bariatric surgery drugs that impair lipid hydrolysis drugs that impair bile acids impaired hepatobiliary system unabsorbed fat substrates
What is the Tx for fat soluble vit deficiencies
make a water-miscible form (can be absorbed by aqueous environment)
What can a folate deficiency cause
neural tube defect in developing fetus
causes spina bifida and anencephaly
What is the biochemical active form of folate and function
tetrahydrafolate
important in DNA synthesis because needed for thymine and purines
What can result from tetrahydafolate or folate deficiency
megaloblastic anemia (RBC are large because uninhibited protein and RNA synthesis)
What is the tx for a folate deficiency
medicinal form of pteroylmonoglutamate (PteGlu1)
What is the food form of folate
polyglutamate (PteGlu7)
What is on the surface of entercyte membrane for folate digestion
folate conjugase that removes glutamate one by one
Where is folate transported into enterocyres
PteGlu1 carrier in SI
Where is folate activated to THf
in the liver
Where is Vit B12 synthesized (cobalamin)
microbes (in animal products so need to be supplemented in vegetarians)
What is Vit b12 a coenzyme for
transfers methyl group to homocystein to make methionine
What is methionine essential for
without it body uses intracellular stores of folate so can also then lead to megaloblastic anemia
Describe absorption of vit B12
starts in stomach because released via pepsin and low pH, bound to haptocorrin in stomach
interacts with IF in SI, the HCO3 release stimulates release of haptocorrin and vit B12 so that IF can bind it
How are Vit B12 absorbed into enterocytes
enterocyte has apical cobalamin-IF Receptor
Once in the enterocyte what happens to Vit B12-IF
dissociate and then Vit B12 binds transcobalamin II to exit basolateral surface
Hpw is Vit B12 taken to liver
hepatic ciruclation
What happens to excess vit B12 once in liver
excreted in bile
What can cause a vit B12 deficiency
can occur from not eating meat can occur from pernicious anemia which happen due to lack of parietal cells bacteria can metabolize it crohn disease ileal reaction
what can lead to lack of parietal cells
atrophy or Ab-mediated immune response agasint parietal cells or IF
no IF secretion
no absorption without IF
