Endogenous lipid transport

Endogenous lipid transport

The apoproteins serve both in the assembly of the lipoproteins and in the determination of their metabolic fate. Several of the apoproteins are ligands for specific cell surface receptors and, as a consequence, facilitate lipid delivery to, and possibly from, cells and control the catabolism of the lipoproteins. The liver synthesizes and releases VLDL into the plasma. At the capillaries, VLDL is depleted of triglycerides by the lipoprotein lipase enzyme (LPL). The formed free fatty acids are transported to muscle and adipose tissue. The remaining VLDL-remnants transport cholesterol further to the liver. VLDL remnants are cleared from the plasma by the LDL-R in the liver. In order to further distribute cholesterol, LDL is synthesized by hepatic lipase (HL). The LDL-R recognizes and

mediates the cellular uptake of lipoproteins containing either apoprotein B-100 or apoE, which are exposed on the surface of IDL and LDL. This LDL-R is localized in the liver, adipocytes, adrenal gland and peripheral tissue. Peripheral cells need cholesterol for cellular processes (formation of membranes, steroid synthesis etc.). Click here for more information on the LDL-R cycle. Excess of cholesterol in the peripheral cells is transported back to the liver by HDL particles. Scavenger receptor class B type I (SR-BI) mediates the selective uptake of HDL into the hepatocyte via the apoprotein A-I on the HDL surface. The excess of cholesterol in the liver is thus secreted as LDL or as bile acid. See next graphic for more explanation of processes in the hepatocyte.


Which of the following is the major carrier for the transport of cholesterol to peripheral tissues?


Which one of the following enzymes is involved in the mobilization of fatty acids from triglycerides stored in adipose tissue? 


All of the following are true statements about lipoprotein lipase activity EXCEPT