Overview Snapshot A 50-year-old woman presents to her primary care physician for a regular checkup. She states that for the past four months she has not experienced menses. Her primary care physician suspects that she has gone through menopause. On routine lab work, her LDL has increased as compared to one year ago, and her HDL has decreased drastically. Introduction Mechanisms for fatty acid and cholesterol transport Different types that vary by density most dense HDL (high density) LDL (low density) IDL (intermediate density) VLDL (very low density) chylomicrons least dense types of apolipoprotein HDL Function transfer cholesterol tissues → liver good cholesterol Structure apoA-1 activates lecithin cholesterol acyltransferase (LCAT) apoE/apoC-II apolipoproteins donated to chylomicrons and VLDL LDL Function transfer cholesterol liver → tissues most recycles back to be absorbed by the liver bad cholesterol Structure apoB-100 mediates endocytosis of LDL by binding to apoB-100 (LDL) receptor on liver and tissues IDL Function VLDL → IDL + TGs picks up cholesterol esters from HDL catalyzed by cholesterol ester transfer protein (CETP) IDL + cholesterol from HDL → LDL Structure apoE recieves from HDL mediates uptake by the liver remember: apoE empties to liver apoB-100 mediates endocytosis of LDL by binding to apoB-100 (LDL) receptor on liver and tissues VLDL Function transports TGs liver → tissues Structure apoB-100 form packaged and secreted from liver apoC-II activates lipoprotein lipase catalyzes hydrolysis of triglycerides into individual FAs for absorbtion ↑ regulated by insulin apoE mediates uptake by the liver Chylomicrons Function transport cholesterol, TGs, FAs, and fat soluble vitamins intestine → tissues released from intestinal lumen cells into lymphatics Structure apo-48 form packaged and secreted by intestine apoC-II activates lipoprotein lipase added from HDL apoE mediates uptake by the liver added from HDL