Week 11 Objectives Flashcards
(9 cards)
Identify the four major groups of plasma lipoproteins and the four major lipid classes they carry.
Chylomicron - most TAGs / intestines
VLDL - mostly TAGs/ liver
LDL - cholesterol esters / nascent VLDLs going past LPL on wall
HDL - protein / liver
• Indicate the major types of apolipoprotein found in the different lipoprotein classes.
CM ApoA, B48, B100, C, E
VLDL ApoB100, C, E
LDL ApoB100
HDL ApoC, E
• Explain that triacylglycerol from the diet is carried to the liver in chylomicrons and from the liver to extrahepatic tissues in very-low-density lipoprotein (VLDL), and that these particles are synthesized in intestinal and liver cells, respectively, by similar processes.
Chylomicrons:
- released into circulation from intestinal cells
- MTP loads ApoB48 on the CM
- nascent chylomicron: in bloodstream
- interacts w HDL: gets ApoCII+E
VLDL:
- released into circulation from liver hepatocytes
- MTP loads ApoB100 on the VLDL
- nascent chylomicron: in bloodstream
- interacts w HDL: gets ApoCII+E
• Illustrate the processes by which chylomicrons are metabolized by lipases to form chylomicron remnants, which are then removed from the circulation by the liver.
ApoCII interacts w/ LPL
- LPL hydrolyzes TAGs->FFAs
- FFAs either oxidizes or stored as TAGs
- Insulin enhances LPL
ApoE on remnants -> liver uptake of SR-B1 receptor
-broken down into C, AA, glycerol
• Explain how VLDL is metabolized by lipases to intermediate-density lipoprotein (IDL) which may be cleared by the liver or converted to low-density lipoprotein (LDL), which functions to deliver cholesterol from the liver to extrahepatic tissues via the LDL (apoB100, E) receptor.
ApoCII interacts w/ LPL.
- VLDL receptor enhances this rxn.
- hydrolyzes TAGs -> FFAs
- FFAs oxidized by muscles or stored as TAGs in adipose
- Insulin enhances LPL
ApoE on IDL (VLDL remnant)
- facilitates liver uptake of SR-B1 receptor
- broken down into C, AA, glycerol
• Explain how high-density lipoprotein (HDL) is synthesized, indicate the mechanisms by which it accepts cholesterol from extrahepatic tissues and returns it to the liver in reverse cholesterol transport.
-HDLs originate in the liver + intestine, ApoA present
-serve as a source of ApoC+E
-ABC transporters: assist in the transport of cholesterol/lipids from the cells -> HDL
-CETP: cholesterol esterase transport protein
*associated with HDL
*exchanges TAGs from VLDL w/ cholesterol ester from
HDL
• Describe how the liver plays a central role in lipid transport and metabolism and how hepatic VLDL secretion is regulated by the diet and hormones.
Liver is where VLDLs and HDLs are formed and the VLDLs would be present in lipid panel after fast, although chylomicron are primary dietary cholesterol carrier.
Insulin inhibits MTP / activates SR-B1 receptor
• Indicate the roles of LDL and HDL in promoting and retarding, respectively, the development of atherosclerosis.
LDL -> high cholesterol -> atherosclerosis
HDL -> low cholesterol -> low risk
Abetalipoproteinemia: loss of ApoB capabilities (loss of CM and VLDL)
Famililal hypercholesterolemia -> loss of LDL receptor -> elevated LDL
• Indicate the causes of alcoholic and nonalcoholic fatty liver disease (NAFLD).
Alcoholic: excess alcohol
Non-alcoholic: high TAGs or LDL/ low HDL and insulin resistance
