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49 Cards in this Set

  • Front
  • Back
1. Where does fat absorption occur?
a. Jejunum
2. What is the specific activity of lipase?
a. Fatty acids from positions 1 and 3 are preferentially removed
b. Leaves 2 FFA and one 2-monoacylglycerol
a. What secretes lingual lipase?
i. Cells at the back of the tongue
b. At what pH does lingual lipase work best? Where is it active?
i. Acidic
ii. Active in stomach
c. Why are lingual lipase and gastric lipase slow?
i. They are active only on the surface of the lipid droplet
d. What physical process increases activity of lingual and gastric lipase?
i. Peristalsis of stomach
a. What is secreted along with pancreatic lipase?
i. Procolipase
b. What is the active enzyme of procolipase? What is the activator?
i. Colipase
ii. Trypsin
c. What is the MOA of colipase?
i. Binds lipase to mixed micelles
ii. Prevents the inhibition of lipase by bile salts
d. What are the major products of pancreatic lipase?
i. FFA
ii. 2-monoacylglycerol
a. In what form is phospholipase A2 secreted? What is its activator?
i. Prophospholipase A2
ii. Trypsin (bile salts required)
b. What is the specific activity of phospholipase A2?
i. Removes one FA molecule from 2 position of phospholipids
ii. Yields one FFA and one lysophospholipid
a. What is the activity of cholesterol esterase?
i. Cholesteryl esters are hydrolyzed to cholesterol and FFA
a. Where are bile salts produced?
i. In the liver
b. From what are bile salts derived?
i. Cholesterol
c. Where are bile salts stored?
i. Gall bladder
d. What does bile contain?
i. Bile salts
ii. Phospholipid
iii. Cholesterol
e. What compounds can form micelles?
i. Bile salt
ii. Phospholipid
iii. Cholesterol
f. What are the steps of micelle formation?
i. Emulsified fat droplet acted on by digestive enzymes
ii. Products of digestion incorporated into bile salt micelles
iii. Micelles can become “mixed”-- contain bile salts, PC, cholesterol, and products of lipid digestion
g. What is the function of mixed micelles?
i. Allow for distribution of products of lipid digestion to intestinal epithelium for absorption
a. What does knockout of NPC1L1 result in?
i. Reduces cholesterol absorption by more than 70%
b. What other enzymes are involved in cholesterol absorption?
ii. CD36
c. Where is ABC transporter located? What is its function?
i. Intestinal epithelial cells
ii. Pump sterols out of the cell
d. What are two ABC transporters?
i. ABCG5
ii. ABCG8
e. How can consuming plant sterols decrease cholesterol absorption?
i. Competing with cholesterol for absorption
ii. Sterols pumped out of intestinal epithelial cell
iii. Less cholesterol absorbed
f. Where are bile salts absorbed?
i. Ileum
g. What is enterohepatic circulation?
i. Return of bile salts to liver by portal circulation
h. Once lipids are absorbed, in what form are they stored?
i. Chylomicrons
i. What is the function of FAB/FAB2?
i. Bind long chain fatty acids
ii. Transport LCFA into endoplasmic reticulum
j. What happens to LCFAs in the ER?
i. Converted to TAGs
k. How are FFAs converted to fatty acyl-CoA?
l. How are most of TAGs synthesized?
Monoacylgycerol pathway
Monoacylgycerol pathway
m. How are the TAGs not synthesized by the monoacylglycerol pathway produced?
i. Phosphatidic acid pathway
n. In what form do short and medium chain fatty acids enter hepatic portal vein? What do they bind to in order to enter the liver?
i. FFA
ii. Subsequently transported to liver bound to albumin
o. How is cholesterol converted to cholesteryl ester?
a. What is the function of apo-proteins?
i. Assist in chylomicron formation
b. What is the major apo-protein? What is it?
i. B-48
ii. Splice-variant of a gene expressed in liver
iii. In intestinal epithelial cells, the splice variant is 48% of that in liver
c. Where are apo-proteins synthesized?
i. RER
d. Where are apo-proteins assembled into the chylomicron assembly?
i. Golgi apparatus
e. Where are chylomicrons secreted?
i. Lymph
a. What is steaorrhea? What causes it?
i. Presence of excess fat in stool (may be greasy or foul smelling)
ii. Symptom of anything which interrupts lipid digestion and/or absorption
b. What causes a bile insufficiency? What is the result?
i. Biliary obstruction or severe liver disease
ii. Steatorrhea results
iii. Clay colored stools
iv. Fat soluble vitamin deficiencies
c. What causes pancreatic enzyme insufficiency? What is the result?
i. Cystic fibrosis or pancreatitis
ii. Steatorrhea results→ decreased absorption of fat and fat soluble vitamins
i. What is the MOA of orlistat?
1. Inhibitor of gastric and pancreatic lipase
ii. What is the aim of orlistat? What are the side effects?
1. Reduce fat absorption by preventing TAG digestion
2. Steatorrhea
i. What is olestra?
1. octa-acyl sucrose
2. Sucrose with a fatty acyl on each hydroxyl group
ii. Why is olestra preferable to “real fat”?
1. Has the taste and consistency of fat but is non-digestible
iii. What is the drawback of olestra? How can you combat them?
1. Fat soluble vitamins can pass through digestive system along with olestra
2. May cause steatorrhea
3. Combat by supplementing with fat soluble vitamins
i. What does ezetimibe do?
1. Inhibits NPC1L1
2. Diminishes cholesterol absorption