HDL and Triglycerides Flashcards
HDL is produced by?
Liver (A-I and A-I/A-II types)
Intestines (A-I type only)
LCAT Function?
lecithin-cholesterol acyltransferase. Converts Free Cholesterol into Cholesteryl Ester (more hydrophobic)
SR-BI Receptor
Scavenger receptor class B member 1. Acts as a receptor for HDL in the liver.
Mature vs Nascent HDL
Cholestyl Ester (CE) vs Free cholesterol (FC)
CETP or PLTP Function
Cholesteryl ester transfer protein (CETP), also called plasma lipid transfer protein (PLTP), is a plasma protein that facilitates the transport of cholesteryl esters and triglycerides between the lipoproteins.
LDR-R Function
Binds LDL/VLDL B Receptor to transfer CE and TG from LDL/VLDL to the liver.
Causes of Low HDL-C
Genetics Insulin Resistance (hypertriglyceridemia, obesity, tobacco) Drugs (sirolimus, B-blockers...) Proteinuria Critical Illnesses
Does increasing HDL-C reduce CVD events?
Not enough evidence to make this a treatable risk factor!
Chylomicron
TG-Rich Lipoproteins
Made in the inestine
Increase after fat intake
May be found in fasting plasma if TGs are >500 mg/dL and always if >1000 mg/dL
VLDL
TG-Rich Lipoprotein
Made in the Liver
Normal TG levels < 150 mg/dL
Increase after carb intake
TGs affect
Women more
AreTriglyceride-Rich Lipoproteins Atherogenic?
Causes Endothelial dysfunction
Arterial retention by LPL
Direct uptake by macrophages → foam cells
Promotion of thrombogenic precursor synthesis
Lp (a) Function
Present at very low to very high levels
Concentration is strongly influenced by hereditary factors
Not influenced by Rx
It is pro-thrombotic and blocks fibrinolysis!!
HDL Function vs Levels
Levels of HDL may be LESS important than the function/ ability of the HDL itself
HDL Treatment
Not a treatment goal for CVD risk reduction!
