lipoprotein metabolism

  1. Does high concentration of cholesterol downregulate or upregulate the production of HMG CoA reductase?
    Downregulate; high cholesterol available there is no need to make more cholesterol
  2. Does high concentration of cholesterol downregulate or upregulate the synthesis of LDL receptor?
    Downregulate
  3. What is HMG CoA reductase involved in?
    Involved in cholesterol synthesis
  4. What does SRE stand for?
    Sterol regulatory element (DNA sequence)
  5. What does SREBP-2 stand for?
    Sterol regulatory element- binding protein 2 (contains a transcription factor)
  6. What does SCAP stand for?
    Sterol regulatory element- binding protein 2 cleavage activating protein
  7. Where do SREBP-2 and SCAP normally reside/sequestered?
    In the endoplasmic reticulum
  8. Where do SREBP-2 and SCAP go before it becomes activated?
    In the golgi (SCAP will cleave and activate SERBP-2 in the golgi)
  9. What is the purpose of SREBP2?
    Fragment (activated SREBP-2) will act as a transcription factor that ultimately leads to HMG CoA reductase synthesis
  10. What happens to SREBP2 and SCAP when there is high cholesterol in the cell?
    They remain trapped inside the endoplasmic reticulum
  11. Does insulin upregulate or downregulate production cholesterol?
    Upregulate production of cholesterol
  12. True/False: Insulin cause Insig to RELEASE SCAP and SREBP in the endoplasmic reticulum which will lead to cholesterol synthesis
    True. Insulin upregulate the production of cholesterol
  13. Does AMP activated kinase upregulate or downregulate the production of cholesterol?
    Downregulate; AMP is high in the cell means there is low energy, when there is low energy cell would not be producing cholesterol
  14. What phosphorylates HMG CoA Reductase?
    AMP activated kinase (AMPK)
  15. What happens when HMG CoA Reducatase is phosphorylated?
    Inactivate HMG CoA reductase and thereby downregulate cholesterol synthesis
  16. What is the regulated step of cholesterol synthesis?
    HMG CoA Reductase
  17. What pharmaceutical inhibit HMG CoA reductase?
    Statin
  18. Inhibiting HMG CoA reductase would have what effect on LDL receptor synthesis?
    Making more LDL receptors which will pull in more cholesterol from blood
  19. Inhibiting HMG CoA reductase would have what affect on liver cell synthesis of cholesterol?
    Decrease
  20. What are the uses for acetyl coenzyme A?
    • Make Carbon-Carbon bonds (high energy)
    • Also medium energy ester bonds
  21. What ie intermediate molecule in the committed step of cholesterol synthesis?
    Beta-hydroxymethylglutaryl coenzyme A
  22. What is the enzyme of the committed step of cholesterol synthesis?
    Beta-hydroxymethylglutaryl-coenzyme A reductase
  23. What is an adverse effect of statin therapy?
    Severe myalgia due to decreased in unbiquinone concentration in muscle
  24. Apo-B48 is found on which lipoprotein?
    Chylomicron
  25. Apo-B100 is found on which lipoprotein?
    VLDL
  26. Apo-A1 is found on which lipoprotein?
    HDL
  27. Which cell releases chylomicrons?
    Enterocytes
  28. Which cell releases VLDLs?
    Hepatocytes
  29. When is the concentration of chylomicrons the highest?
    Postprandially
  30. Which is more dense: protein or lipid?
    Protein is denser than lipid
  31. Which is more dense: cholesterylesters or triacylglycerols?
    Cholesterylesters are more dense than triacylglycerols
  32. Rank the lipoproteins from least to most dense:
    Chlyomicron < VLDL
  33. True/False: chylomicrons readily enter and leave the tunica intima (endothelial lining of arteries)
    False; chylomicrons are too large to do that, they do not enter. LDLs enter and leave most readily
  34. What does HDL transport and where does it transport it to?
    HDL transport cholesterol from the tunica intima of blood vessels out to the liver for processing for other uses
Author
lykthrnn
ID
344942
Card Set
lipoprotein metabolism
Description
cardiovascular final
Updated