Liver secretes very low density lipoproteins (VLDL) containing mainly TG and some CHE into blood. VLDL is acted upon by endothelial lipoprotein lipase in the same way as on Chy and the fatty acids pass into adipose tissue and muscle; the remnant called intermediate density lipoprotein (IDL) now contains more CHE than TG. About half of the IDL is taken back by the liver cells by attachment to another receptor (LDL receptor), while the rest loses the remaining TGs gradually and becomes low density lipoprotein (LDL) containing only CHE. The LDL circulates in plasma for a long time; its uptake into liver and other tissues is dependent on the need for CH. The rate of LDL uptake is regulated by the rate of LDL receptor synthesis in a particular tissue.

The CHE of LDL is deesterified and used mainly for cell membrane formation. The CH released into blood from degradation of membranes is rapidly incorporated in high density lipoproteins (HDL), esterified with the help of an enzyme lecithin cholesterol acyltransferase (LCAT) and transferred back to VLDL or IDL, completing the cycle.

The excess lipoproteins in plasma are phagocytosed by macrophages for disposal. When too much of lipoproteins have to be degraded in this manner, CH is deposited in atheromas (in arterial walls) and xanthomas (in skin and tendons). Raised levels of VLDL, IDL and LDL (rarely Chy and Chy. rem, also) are atherogenic, while HDL may be protective, because HDL facilitates removal of CH from tissues.

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