Chylomicrons are formed in the intestine from ingested fat and taken by the intestinal lymphatics to peripheral blood and then to adipose and other tissues. There, most of the triglyceride is acted upon by the enzyme lipoprotein lipase, transported across the cell membrane as fatty acid and monoglyceride, resynthesized into triglyceride, and stored. When necessary, intra-cellular triglyceride can undergo lipolysis. The released fatty acid is then transported out of the cell and bound to albumin to be transported in the plasma. After lipolysis a remnant of the chy-lomicron is transported to the liver and catabo-lized as a portion of the particle apolipoprotein A [Apo(A)] free cholesterol, and phospholipid is transferred to HDL formed in the liver; HDL may also pick up free cholesterol from cells. The cholesterol from other cells is esterified under the influence of LCAT. This ester is then available for storage or transport.
Very low-density lipoprotein is synthesized in the liver from fatty acids obtained from the processing of chylomicrons or from endogenously produced triglyceride. These particles are smaller and more dense than chylomicrons. The apolipoproteins associated with VLDL are Apos B-100, C-1, C-II, C-III, and E.
Very low-density lipoprotein exchanges triglycerides for cholesterol esters from HDL. Like chylomicrons, lipoprotein lipase catalyzes the hydrolysis of triglyceride in VLDL to fatty acids that are used by muscle or stored as fat in adipose tissue. This hydrolysis step reduces VLDL to IDL. Intermediate-density lipoprotein can be taken up by the LDL receptor or be reduced to LDL by hepatic lipase. Intermediate-
density lipoprotein clearance is mediated by Apo E, which has a higher affinity for the LDL receptor than Apo BB. Low-density lipoprotein contains only the apolipoprotein B-100. Two thirds of the LDL is cleared through the LDL receptor, 60% to 70% of which is located in the liver. Peripheral cells can also take up LDL for membrane biogenesis and steroid synthesis.
Low-density lipoprotein is removed from plasma by binding to these specific receptors located in many tissues, including the liver. After binding, LDL is internalized and metabolized to free cholesterol and other products. Cholesterol is stored in cells as the ester. Saturation of LDL receptors inhibits intracellular cholesterol synthesis by inhibiting HMG CoA reductase. This negative feedback system operates so that intra-cellular cholesterol synthesis varies inversely with the availability of intracellular LDL.
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