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45 Cards in this Set
- Front
- Back
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1. What is the subcellular location of cholesterol?
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a. Cytosol
b. ER |
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2. What is the substrate for cholesterol synthesis?
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a. Acetyl-CoA
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3. What reduces HMG-CoA to mevalonate?
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a. HMG-CoA reductase
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4. What is the importance of HMG-CoA reductase?
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a. It is the major control point for cholesterol synthesis
b. Inhibited by statins |
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5. What is the location of HMG-CoA reductase?
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a. ER membrane
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6. How is isopentenyl diphosphate formed from mevalonate?
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a. Sequential phosphorylation by 3 kinases
b. Decarboxylation |
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7. How is squalene formed from geranyl diphosphate?
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a. 2 isoprenoid units are used to form geranyl diphosphate
b. A third isoprenoid unit is added to form farnesyl diphosphate c. Two farnesyl diphsophates are used to synthesize squalene |
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8. How is lanosterol formed from squalene?
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a. Squalene epoxidase requires NADPH and O2
b. Lanosterol represents the first sterol produced in the pathway to cholesterol |
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9. How is cholesterol formed from lanosterol?
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a. Removal of methyl group at C14
b. Removal of two methyl groups at C4 c. Reduction of the C24 double bond d. Moving the delta 8,9 bond to delta 5,6 |
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10. Where does the conversion from lanosterol to cholesterol occur?
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a. ER
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11. How are prenylated proteins formed?
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a. GTP binding proteins are prenylated with either farnesyl or geranygeranyl residues
b. Residues may anchor protein to the membrane |
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12. How is dolichol formed?
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a. Formed from farnesyl diphosphate plus up to 16 more isopentenyl residues
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13. What is the importance of dolichol?
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a. Required for synthesis of N-linked glycoproteins
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14. How is ubiquinone formed?
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a. From farnesyl disphosphate plus 3-7 isopentenyl residues
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15. What is the importance of ubiquinone?
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a. Required for ETC
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16. What is ACAT? What does it catalyze?
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a. Acyl CoA-cholesterol acyltransferase
b. Formation of cholesteryl ester |
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17. What happens to cholesteryl ester once it is formed?
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a. Packaged into VLDL
b. Stored into liver for future use |
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18. What is the use of cholesteryl esters once they are transferred to other tissues?
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a. Steroid hormone synthesis
b. Vitamin D synthesis |
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19. Where does cholesterol from the liver go?
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a. May be secreted into bile
b. May be synthesized to bile acids and their salts |
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20. How is 7α-hydroxycholesterol formed from cholesterol?
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a. 7α-hydroxylase as catalyst
b. Requires NADPH, O2, CP450, vitamin C |
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21. What is the committed step of bile acid synthesis?
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a. Cholesterol to 7α-hydroxycholesterol
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22. How are cholic acid and chenodeoxycholic acid formed from 7α-hydroxycholesterol?
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a. 12α-hydroxylase as catalyst
b. Propionyl-CoA obtained from carbons removed to form acids c. Require NADPH, O2, and CoA |
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23. Which predominates in humans, cholic acid or chenodeoxycholic acid?
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a. Cholic acid
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24. What happens to cholic acid and chenodeoxycholic acid once they are formed?
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a. They are conjugated with glycine or taurine
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25. What happens once cholic acid and chenodeoxycholic acid are conjugated?
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a. Four primary bile acids are formed
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26. What are the four primary bile acids?
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a. Taurocholic acid
b. Glycocholic acid c. Taurochenodeoxycholic acid d. Glycochenodeoxycholic acid |
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27. What does the formation of the primary bile acids require?
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a. Cholyl-CoA
b. Chenodeoxycholyl-CoA |
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28. What happens to the primary bile acids once they are formed?
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a. They are secreted into the liver with cholesterol
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29. How are the primary bile acids metabolized by intestinal bacteria? What results?
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a. Deconjugation, 7α-dehydroxylation
b. Secondary bile acids |
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30. What are the secondary bile acids?
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a. Deoxycholic acid
b. Lithocholic acid |
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31. Where are both primary and secondary bile acids reabsorbed? What happens to them thereafter?
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a. Ileum
b. Returned to liver to become conjugated and secreted→ enterohepatic circulation |
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32. What controls whole-body cholesterol metabolism?
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a. Liver
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33. How does the liver receive excess cholesterol from body tissues?
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a. LDL receptors
b. Reverse cholesterol transport |
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34. What are the major regulatory targets of the liver to regulated cholesterol metabolism?
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a. HMG-CoA reductase→ major point
b. LDL receptor c. 7α-hydroxylase |
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35. What stimulates transcriptional control of HMG-CoA reductase?
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a. Binding of SREBP to SRE of HMG-CoA reductase
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36. What do elevated levels of cholesterol in the cell do to the SREBP/SRE interaction?
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a. Prevents SREBP from binding to SRE
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37. How does SREBP overcome high cholesterol levels in the cell?
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a. SREBP binds to SCAP in the ER membrane
b. SCAP/SREBP complex kept in ER by cholesterol bond to SCAP c. Cholesterol levels drop, cholesterol leaves the SCAP binding site d. SREBP/SCAP moves to the Golgi e. SREBP goes through proteolysis, N-terminal SREBP free to travel to bind the SRE |
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38. What happens to HMG-CoA reductase when bound to cholesterol?
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a. More susceptible to proteolysis
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39. What is the effect of phosphorylation on HMG-CoA reductase?
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a. Less active
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40. What factors promote phosphorylation of HMG-CoA reductase?
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a. Glucagon
b. Glucocorticoids c. Cholesterol |
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41. What factors promote dephosphorylation of HMG-CoA reductase?
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a. Insulin
b. Thyroid hormone |
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42. What regulates the number of LDL receptors?
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a. Intracellular cholesterol content
b. By same mechanism as SREBP |
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43. What will increased bile acids in the liver repress? How?
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a. 7α-hydroxylase
b. Bile acids bind the farnesyl X receptor c. FXR/bile acid complex suppresses 7α-hydroxylase |
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44. What are the components of cholesterol stones?
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a. Cholesterol
b. Ca salts c. Bile pigments d. Proteins e. FA |
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45. What are the components of pigment stones?
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a. Calcium bilirubinate
b. <20% cholesterol |
