Cholesterol (C), Triglycerides (TGs), Lipoproteins (LPs), and apolipoproteins (ALPs)
What is cholesterol for?
cell membranes (steroid hormones - cortisol)
What are TGs for?
nutrients (energy)...they carry fatty acids
What are the sizes of LPs?
chylomicrons > chylomicron remnants > VLDL > IDL > LDL > HDL VLDL is made by liver. IDL is metabolized to LDL metab to HDL
What are apolipoproteins?
"biochemical keys" - allow LP access to specific sites for delivery, modification
What is exogenous lipid metabolism?
Dietary fats acquire APLs (from HDL) to form chylomicrons. TGs hydrolyzed by lipoprotein lipase (LPL) to free fatty acids to go to adipose/storage or muscle/energy.
The do not contribute to AS, but remnants removed by liver can be taken up by macrophages and contribute to AS.
What is endogenous lipid metabolism?
Fats into liver are either stored or exported as VLDL (not atherogenic). LPL act on VLDL>>>fatty acids released into tissues & VLDL metab to IDL (not atherogenic). IDL metab to LDL in liver which has C & LPs, but no TGs. Most LDL is taken up by liver, but some to tissues>>>taken up by macrophages, oxidized and contribute to AS. (LDL is seen more in pts w/high TGs)
What is a rare genetic defect in RCT (reverse cholesterol transport)?
CETP(C ester transfer protein) defect which is high HDL but high CV events
What are lipid-activated nuclear receptors?
Fibrates activate PPARs (peroxisome proliferator-activated receptors) which accelerate fatty oxidation in liver & elevate HDL. Glitazones active PPARs in muscle/adipose. PPAR agonists & CETP inhibitors have no benefit.
What do Liver X receptors do?
They promote FA & TG synthesis and stim conversion of C to bile acid.
What does niacin do?
Blocks release of FA from adipose.
What does resins do?
Decrease bile acids from being absorbed>>> dec C in liver>>>in LDL receptors in liver>>> dec LDL (but inc TGs)