P2- Dyslipidemia exam 2

Essential for HDL production

Defects in ApoA1 are associated with atherosclerosis

ApoB100 is key characteristic for LDL

used for structural stability & as a ligand for LDL receptor on liver

ApoB100 is associated with hypercholesterolemia

ApoCII a ligand used to bind to LPL receptor in tissues

Defects are associated with hypertriglyceridemia

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

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

Packaged in the ER of liver into chylomicrons

Form TG for storage

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

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

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

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

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