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Lecture 19

BIOCHEM 4M03 Lecture Notes - Lecture 19: Apolipoprotein A1, Very Low-Density Lipoprotein, Lipoprotein

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Deborah Sloboda

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Biochem 4M03 Lecture 19 Lipoproteins: Atherosclerosis & CVD
- 1) LPL hydrolyzes TAG
- 2) Fatty acids can enter tissues or circulation
- 3) Other lipases (HSL) can hydrolyze TAG inside of cells
o LPL penetrate and access lipids on the inside
- Lipoprotein structure
o HDL has ApoA, targeting it for certain processes
o LDL, VLDL tend to have apoB
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- LDL receptor (LDLr)
o Can measure LDL to HDL ratios
o LDL marks how much is out in liver through detection system
o Liver has receptors for ApoB100 on membrane
o Cholesterol can be excreted
o This is the major excretion system for cholesterol (has to come back to the liver)
o Can be stored, used, reused in the liver
o These vesicles responsible for this continually cycles between begin on
membrane and inside cell
o There are drugs that keep receptors out a membrane longer to capture more LDL
(ex. Lipitor)
- HDL: Reverse Cholesterol Transport
o Need capture system that takes it back to liver
o After efflux cholesterol, binds to HDL to digest it off
o Sequester to HDL to excrete it in bile
o Need to reproduce major steps in this process
o This whole process is the reverse cholesterol transport
Question: LCAT?
- Cholesterol tends to be inside
- LCAT = Lecithin cholesterol acyltransferase
- Catalyzes cholesterol cholesterol ester
- Cholesterol esters have lower solubility
- Increased hydrophobicity promotes sequestration inside lipoprotein
- More “protected” and suitable to transport back for excretion
- LCAT makes cholesterol into cholesterol ester and packs it on inside so it’s more
protected and can make its way back into liver
- Enzyme helps for HDL molecule
- Atherosclerosis and cardiovascular disease is separate
o Atherosclerosis is biological process
- Cardiovascular disease is the leading cause of mortality in the world
- Atherosclerosis is the accumulation of lipid (TAG & cholesterol), immune cells and
fibrous debris in the intimal space of coronary and larger arteries
- Multi-factorial (genetic/environmental)
- Plaque buildup causes dysfunction of heart or what it feeds
- Interested in atherosclerotic plaque
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