(See the whole sequence of lipoprotein interconversions.)

Clicking on an *asterisked* word below takes you to that apoprotein.

  Apo B is incorporated into VLDL by hepatocytes, preparing this lipoprotein for transport of triglycerides (TG) and cholesterol from liver to other tissues. The VLDL as it is secreted is in an incomplete *nascent* state.
  The conversion of nascent VLDL to its functional form needs the addition of Apo E and Apo C2 donated by *HDL* which in turn acquires them from other lipoproteins to form the "mature" *VLDL* that transports lipids.
×××××
  When VLDL encounters lipoprotein lipase *LPL* in tissue capillaries the Apo C2 on the VLDL activates the enzyme, which hydrolyzes much of the triglyceride of the VLDL to produce *IDL*. The latter releases Apo C2 and Apo E which are recycled to HDL and then to VLDL.
×××××
  About 1/2 of the resulting IDL, which is poorer than VLDL in triglyceride and relatively richer in cholesterol and its esters, is taken up by the liver by a receptor that recognizes the *Apo B* of the IDL.
The *LDL* is taken up by the liver with its Apo B acting as the ligand to the receptor. Another 24% of the LDL is delivered to *other tissues* leaving about 1% of the LDL to be removed from the circulation by scavenger cells such as those found in atheromatous plaques.
×××××
  However, the receptors on scavenger cells do not recognize "native" Apo B. Rather, they have a specific affinity for *oxidized* Apo B which is formed when LDL persists for an abnormally long time in the circulation.
×××××
  Persistence of LDL in the circulation may result from the excessive VLDL production associated with a high dietary intake of fats, especially those rich in saturated fatty acids. It also occurs in primary and secondary lipidemias in which there is a subnormal uptake of IDL and LDL by the liver and other tissues.
×××××