Transport of lipophilic substances in watery media like blood or lymphatic fluid is dependent on the formation of particles with hydrophilic surfaces. This is achieved with the help of apoproteins (A, B48, B100, C, and E). Their amphipathic structure allows them to mediate between the lipophilic particle cores and the hydrophilic medium. Depending on apoprotein compositions, different transport particles result. Apoproteins also function as markers for specific receptors in the tissues. Even enzymatic digestion of particles is determined by apoproteins.
The lipoproteins formed in this way can be distinguished by their density, which is a function of their different contents in lipids and proteins. Chylomicrons consist mostly of lipids and have a density of <0.95 g/cm3. The lipoprotein protein content and density begins at "very low-" (VLDL), increases through "intermediate-" (IDL) through "low-" (LDL), to "high-density lipoproteins" (HDL). At the same time, particle size decreases from chylomicrons (max. 600 nm after high level lipid absorption) to HDL (-10 nm).
Individual lipoproteins are not static entities. Rather, they represent a continuum and are converted into one another (A). Inside the plasma, this process ensures controlled distribution and release of lipids to the tissues.
(CM) make contact with a lipoprotein lipase (LPL), which is bound to the surface of blood vessel endothelial cells via heparan sulfate. The LPL hydrolyzes triglycerides in positions 1 and 3, releasing fatty acids from the lipopro-teins, most of which are absorbed into the endothelial cell. LPL activity can be regulated via insulin and catechol-amines so that fatty acids can be made available to muscles for energy, or to fatty tissue for triglyceride synthesis, in a targeted fashion.
During this lipolysis, the chylomicrons also lose apoprotein CII. The resulting chylomicron remnants (REM) are recognized (ApoE receptor), endocytosed, and metabolized by hepatocytes. The liver also packages its newly synthesized or recycled lipophilic products into transport particles (n-VLDL); after enrichment with ApoC, they are available to the LPL as VLDL. During hydrolysis by LPL, particles not only lose triglycerides, but also ApoC, among others, making the resulting IDL a poor substrate for LPL. They are, therefore, taken up by hepatocytes (apo-receptors) or further metabolized to LDL under loss of ApoE. LDL particles, the cores of which consist primarily of cholesterol, are absorbed by most peripheral tissues through LDL-recep-tor-mediated endocytosis.
Chylomicrons (n-CM) released from the enterocytes reach the vena cava through the lymphatic vessels. During this passage they already interact with other lipoproteins, exchanging fatty acids and taking up additional apopro-teins.
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