10/21 Transport of Lipids Flashcards
fxn of fibrates
increase LPL expression via PPAR-a so TGs are broken down in the blood to FAs
side effects: gallstones and myalgia
VLDL creation
in the liver, TGs are packed around ApoB-100 by MTP
ezetimibe
inhibits uptake of cholesterol from gut lumen by enterocytes
what other labs can hypertriglyceridemia fuck up
increase in VLDL, increase in LDL, increase in cholesterold deposits in blood vessels
HDL role
cholesterol from peripheral tissues to liver, prevents improper accumulatio of cholesterol, gives ApoCII and ApoE to other lipoproteins
IDL role
when LPL breaks down VLDL, most FAs go into cells, but remaining clump in blood is now called intermediate density lipoprotein. either go to liver for breakdown or become LDL.
cholesterol rich, has ApoE
LDL role
from IDL that has returned to the liver, hepatic lipase removes more TGs, now even denser = LDL, delivers C and CE to tissues with LDL receptors
has least amount of TGs
atherosclerosis
deposition of LDL in vessel walls can lead to lesions, foam cells, inflammation, smooth m hyperplasia, fibrosis
ApoB-100
contains ligand for LDL receptors on liber, main building block of VLDL in liver
MTP
packs VLDL in liver
defect: abetalipoproteinemia (cal deficit, night blindness, spinal and neural defects, acanthocytes, vomiting
LPL
releases FAs from VLDL in blood
requires ApoCII
(+) insulin, fibrates
ApoA-1
building block for HDL in liver
LCAT
picked up by HDL in the blood, allows HDL to pick up C, internalize them, and make them CEs
CETP
exchanges TGs (from chylomicrons and VLDLs) for CEs (from HDL)