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12 Cards in this Set
- Front
- Back
ApoA1
(defects) |
Essential for HDL production
Defects in ApoA1 are associated with atherosclerosis |
|
ApoB
(defects) |
ApoB100 is key characteristic for LDL
used for structural stability & as a ligand for LDL receptor on liver ApoB100 is associated with hypercholesterolemia |
|
ApoC
(defects) |
ApoCII a ligand used to bind to LPL receptor in tissues
Defects are associated with hypertriglyceridemia |
|
ApoE
(defects) |
ApoE used as ligand to bind to LDL receptor on the liver
Also binds to heparin sulfate proteoglycans which allow hepatic lipase to remove TG Defects are associated with hyperlipoproteinemia |
|
Cholesterol
|
Synthesized from dietary fatty acids and or is biosynthesized
Enters the intestine via NPC1L1 transporter Esterification via ACAT2 enzyme yields a cholesterol ester in the liver & intestines |
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Cholesterol Esters
|
Packaged in the ER of liver into chylomicrons
|
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Fatty acids
|
Form TG for storage
|
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Triglycerides
|
Are formed when OH groups on Glycerol react with COOH in fatty acids
TG undergo lipolysis to yield fatty acids for energy Transported by lipoproteins and are either utilized or stored in the liver, adipose tissue, or skeletal muscle |
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Chylomicrons
|
Made in the intestine, exit and enter circulation
Receive ApoC & ApoE from generous HDL ApoC binds to LPL in tissue (adipose & skeletal muscle) and gives away TG |
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Chylomicron Remnants
|
Produced in liver from chylomicrons
Go to liver and bind to LDL or LRP receptor via ApoE ApoE then binds to heparin sulfate proteoglycan to get rid of more TG via hepatic lipase |
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VLDL
|
Produced in the liver from chylomicron
Leaves the liver and gains ApoC and ApoE from generous HDL In the tissues ApoCII binds to LPL where TG are given up |
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IDL
|
Formed in the tissues from VLDL
Has 2 options: either circulate or go back to liver What decides its fate is the number of LDL receptors on liver or number of LPL proteins in tissue |