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34 Cards in this Set
- Front
- Back
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1. What do blood lipoproteins do?
How are they classified? |
Transport water-insoluble TGs and cholesterol from one tissue to another
In terms of density LDL (low density) HDL (high density) |
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2. Where are chylomicrons produced?
What do they carry? |
Intestinal epithelial cells from dietary fat
Triacylglycerols in blood |
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3. Where are VLDL produced?
What do they carry? |
Liver mainly from dietary carbohydrates
Triacylglycerol in blood (de novo synthesis of TG) |
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4. Where are IDL produced?
What happens to them? |
Blood (remant of VLDL after TG digestion)
Endocytosed by liver or converted to LDL |
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5. Where are LDL produced?
What do they contain? What happens to them? What are they called? |
Blood (remnant of IDL after TG digestion)
High concentration of cholesterol and cholesterol esters Endocytosed by lived and peripheral tissue "Bad" cholesterol |
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6. Where are HDL produced?
What do they do? What are they call? |
Liver and intestine
Exchange proteins in lipids w/ other lipoproteins Functions in the return of cholesterol from peripheral tissues to the liver (get rid of cholesterol) "Good" cholesterol |
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7. What is the structure of lipoproteins?
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1. Phospholipids and proteins on surface w/ hydrophilic regions interacting w/ water
2. Hydrophobic molecules in interior 3. Hydroxyl group (OH) is near surface |
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8. In cholesterol esters what happens to the OH group?
Where are cholesterol esters found? |
Esterified to a FA
Interior of lipoproteins |
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9. What are the major functions of the following apoproteins...
1. A-I 2. B-100 3. C-I 4. C-II |
1. Structural, activator of LCAT
2. Structural, ligand for LDL receptor, secretionof VLDL 3. Activator of LCAT 4. Activator of lipoprotein lipase |
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10. What happens to dietary cholesterol?
What does this cholesterol combine with? What is formed and where does it go? |
Absorbed from bile salt micelles into intestinal epithelial cells
Dietary TGs, phospholipids, and apoprotein B Nascent chylomicrons that enter blood via lymph system |
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11. What happens to the nascent chylomicrons once in the lymph and blood?
What does it obtain in order to do this? |
Converted into chylomicorns
Apoprotein CII and apoprotein E from HDL |
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12. In the blood, what happens to chylomicron TGs?
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Digested by lipoprotein lipase (LPL)
Resulting chylomicron remnants bind to receptors on liver cells and are internalized via endocytosis |
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13. What happens to the chylomicron remnants once in the liver cell?
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Digested in lysosomes where cholesterol esters are converted to FAs and free cholesterol
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14. What does the resulting increase in free cholesterol in liver cells do?
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1. Inhibits endogenous cholesterol synthesis
2. Inhibits LDL receptor synthesis *this decreases extracellular uptake of cholesterol via LDL receptors |
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15. How is VLDL formed?
What happens to VLDL? |
Combination of....
1. Liver cholesterol (both de novo synthesis and digestion of blood lipoproteins) 2. TG 3. Phospholipids 4. Apoprotein B-100 Secreted into the blood |
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16. In the blood, what does HDL do?
Once this happens what occurs next? |
Transfers cholesterol esters, apoCII and apoE to VLDL
VLDL is converted to IDL **result of digestion of its TGs by LPL (lipoprotein lipase) |
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17. What can happen to IDL?
Two fates.... |
1. Taken up by liver via receptors
-return VLDL cholesterol back to liver 2. Converted to LDL -hepatic triacylglycerol lipase (HTGL) |
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18. What can happen to LDL?
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1. Deliver cholesterol to peripheral (nonhepatic) cells/tissues
2. Go back to liver **both occur via receptor-mediated endocytosis |
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19. What can happen to oxidized LDL?
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Can be taken up via nonspecific scavenger receptors on macrophages
These macrophages are referred to as "foam cell" |
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20. What do foam cells play a role in?
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Atherosclerosis
**B/c of this, LDL cholesterol is considered "bad" cholesterol |
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21. What does lipoprotein lipase (LPL) do?
Where is this enzyme attached? What activates LPL? What stimulates adipose cells to synthesize and secrete LPL? |
Hydrolyzes lipoprotein TGs in chylomicrons and VLDL to FAs and glycerol
Endothelial cells of capillaries in muscle and adipose tissue ApoCII Insulin *diabetic patients cannot metabolize chylomicrons or VLDL b/c don't have sufficient insulin to stimulate LPL |
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22. Where do LDL receptors exist?
Where is it synthesized and travels to? What does it bind? |
In live and other tissues
Synthesized in ER and Golgi Travels to cell plasma membrane VLDL, IDL, LDL, and chylomicron remnants |
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23. What happens upon binding to LDL receptors?
Once in the endosomes what happens (how are receptors brought back to the surface)? |
Lipoproteins are internalized via endocytosis
1. Decrease in pH 2. Lipoprotein dissociates from receptor 3. Receptors are recycled to cell surface by lipid vesicles |
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24. Why would extrahepatic cells want to take up and degrade LDL?
What do cells use cholesterol for? (four things...) |
Want to keep cholesterol levels constant
1. Maintain cell membranes 2. Repress synthesis of HMG-CoA reductase 3. Stimulate storage of cholesterol as cholesterol esters via ACAT 4. Repress synthesis of LDL receptor protein |
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25. What is LDL receptor-related protein (LRP)?
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Structurally related to LDL receptor
Recognizes broader spectrum of ligands Synthesis of LRP is not affected by intracellular concentration of cholesterol |
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26. Which apoproteins does HDL contain?
What does HDL transfer and to what? |
apoA, apoCII, apoE
apoCII and apoE to chylomicrons and VLDL Also tranfers cholesterol esters (made from cholesterol picked up from cell membranes) to VLDL in exchange for TG |
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27. What facilitates the transfer of cholesterol ester to VLDL?
What happens to HLD as if fills w/ cholesterol ester and TG |
Cholesterol ester transfer protein (CEFP)
Becomes large and spherical |
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28. What is "reverse cholesterol transport"?
Why is HDL "good" cholesterol? |
Cholesterol, collected by HDL from plasma membrane of peripheral cells and from other lipoproteins, is returned to the livers
In the liver, cholesterol esters can be converted to bile salts and eliminated from body in feces |
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29. What is atherosclerosis?
What is the first step in atherosclerosis? |
Plaque formation on inner walls of blood vessels
Formation of foam cells -macrophages engorged w/ lipids from taking up oxidized LDL |
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30. What stimulates formation of oxidized LDL?
What inhibits it? |
Superoxides (H2O2)
Vitamins (E, C, A) |
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31. What are the two next stages of atherosclerosis?
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1. Formation of fatty streaks
-accumulation of foam ceels in subendothelial space of arteries 2. Endothelial cell damage and release of thromboxane A2 (TXA2) -due to extensive fatty streak formation |
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32. What does TXA2 stimulate?
What do both platelets and macrophages release? What does this cause? |
Platelet aggregation
Growth hormone Proliferation and migration of smooth muscle cells to the intimal layer of the arterial wall |
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32. What happens next in atherosclerosis?
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Fibrous plaque formation
-Cells secrete fibrous material that forms a cap -Cells are trapped and begin to die |
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33. What happens when there is an advanced lesion?
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Dead tissue and lipids accumulate
Calcification and hemorrhaging occur Get myocardial infarction b/c blood vessels are being blocked |
