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49 Cards in this Set
- Front
- Back
1. Where does fat absorption occur?
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a. Jejunum
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2. What is the specific activity of lipase?
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a. Fatty acids from positions 1 and 3 are preferentially removed
b. Leaves 2 FFA and one 2-monoacylglycerol |
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a. What secretes lingual lipase?
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i. Cells at the back of the tongue
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b. At what pH does lingual lipase work best? Where is it active?
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i. Acidic
ii. Active in stomach |
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c. Why are lingual lipase and gastric lipase slow?
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i. They are active only on the surface of the lipid droplet
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d. What physical process increases activity of lingual and gastric lipase?
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i. Peristalsis of stomach
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a. What is secreted along with pancreatic lipase?
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i. Procolipase
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b. What is the active enzyme of procolipase? What is the activator?
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i. Colipase
ii. Trypsin |
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c. What is the MOA of colipase?
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i. Binds lipase to mixed micelles
ii. Prevents the inhibition of lipase by bile salts |
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d. What are the major products of pancreatic lipase?
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i. FFA
ii. 2-monoacylglycerol |
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a. In what form is phospholipase A2 secreted? What is its activator?
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i. Prophospholipase A2
ii. Trypsin (bile salts required) |
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b. What is the specific activity of phospholipase A2?
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i. Removes one FA molecule from 2 position of phospholipids
ii. Yields one FFA and one lysophospholipid |
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a. What is the activity of cholesterol esterase?
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i. Cholesteryl esters are hydrolyzed to cholesterol and FFA
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a. Where are bile salts produced?
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i. In the liver
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b. From what are bile salts derived?
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i. Cholesterol
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c. Where are bile salts stored?
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i. Gall bladder
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d. What does bile contain?
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i. Bile salts
ii. Phospholipid iii. Cholesterol |
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e. What compounds can form micelles?
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i. Bile salt
ii. Phospholipid iii. Cholesterol |
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f. What are the steps of micelle formation?
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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 |
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g. What is the function of mixed micelles?
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i. Allow for distribution of products of lipid digestion to intestinal epithelium for absorption
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a. What does knockout of NPC1L1 result in?
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i. Reduces cholesterol absorption by more than 70%
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b. What other enzymes are involved in cholesterol absorption?
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i. SCARB1
ii. CD36 |
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c. Where is ABC transporter located? What is its function?
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i. Intestinal epithelial cells
ii. Pump sterols out of the cell |
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d. What are two ABC transporters?
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i. ABCG5
ii. ABCG8 |
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e. How can consuming plant sterols decrease cholesterol absorption?
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i. Competing with cholesterol for absorption
ii. Sterols pumped out of intestinal epithelial cell iii. Less cholesterol absorbed |
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f. Where are bile salts absorbed?
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i. Ileum
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g. What is enterohepatic circulation?
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i. Return of bile salts to liver by portal circulation
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h. Once lipids are absorbed, in what form are they stored?
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i. Chylomicrons
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i. What is the function of FAB/FAB2?
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i. Bind long chain fatty acids
ii. Transport LCFA into endoplasmic reticulum |
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j. What happens to LCFAs in the ER?
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i. Converted to TAGs
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k. How are FFAs converted to fatty acyl-CoA?
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l. How are most of TAGs synthesized?
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Monoacylgycerol pathway
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m. How are the TAGs not synthesized by the monoacylglycerol pathway produced?
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i. Phosphatidic acid pathway
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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?
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i. FFA
ii. Subsequently transported to liver bound to albumin |
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o. How is cholesterol converted to cholesteryl ester?
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a. What is the function of apo-proteins?
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i. Assist in chylomicron formation
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b. What is the major apo-protein? What is it?
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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 |
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c. Where are apo-proteins synthesized?
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i. RER
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d. Where are apo-proteins assembled into the chylomicron assembly?
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i. Golgi apparatus
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e. Where are chylomicrons secreted?
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i. Lymph
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a. What is steaorrhea? What causes it?
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i. Presence of excess fat in stool (may be greasy or foul smelling)
ii. Symptom of anything which interrupts lipid digestion and/or absorption |
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b. What causes a bile insufficiency? What is the result?
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i. Biliary obstruction or severe liver disease
ii. Steatorrhea results iii. Clay colored stools iv. Fat soluble vitamin deficiencies |
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c. What causes pancreatic enzyme insufficiency? What is the result?
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i. Cystic fibrosis or pancreatitis
ii. Steatorrhea results→ decreased absorption of fat and fat soluble vitamins |
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i. What is the MOA of orlistat?
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1. Inhibitor of gastric and pancreatic lipase
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ii. What is the aim of orlistat? What are the side effects?
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1. Reduce fat absorption by preventing TAG digestion
2. Steatorrhea |
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i. What is olestra?
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1. octa-acyl sucrose
2. Sucrose with a fatty acyl on each hydroxyl group |
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ii. Why is olestra preferable to “real fat”?
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1. Has the taste and consistency of fat but is non-digestible
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iii. What is the drawback of olestra? How can you combat them?
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1. Fat soluble vitamins can pass through digestive system along with olestra
2. May cause steatorrhea 3. Combat by supplementing with fat soluble vitamins |
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i. What does ezetimibe do?
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1. Inhibits NPC1L1
2. Diminishes cholesterol absorption |