The fractional catabolic rate (FCR) for
low density lipoprotein (
LDL)
apolipoprotein B (
apo B) was studied to explore the variations in
apo B as a possible cause of
hypercholesterolemia. The FCR of radioiodine labelled autologous
LDL and homologous
LDL isolated from a normocholesterolemic subject were compared in forty-nine type II hypercholesterolemic males and females with the mean plasma concentration of total
cholesterol of 7.78 mmol/l,
LDL-cholesterol 5.41 mmol/l and
triglycerides 2.09 mmol/l. In most patients the autologous
LDL was catabolized at an equal rate and sometimes even faster than the homologous
LDL. However, twelve out of forty-nine patients catabolized homologous
LDL 0.8-19.3% faster than autologous
LDL and several
apo B polymorphisms were determined. No apo B-3500 or apo B-3531 mutations were detected. Patients with XbaI -/- (absence of cutting site) had lower total, IDL and
LDL cholesterol and
LDL apoB than the other genotypes. Patients with EcoRI +/+ (presence of cutting site) had higher total, VLDL and
LDL cholesterol and slower FCR for autologous
LDL, and their VLDL was richer in
cholesterol than that of patients with the EcoRI +/-. The MspI and ins/del polymorphisms were not associated with variations in the measured parameters. The
apo E 4 was associated with higher VLDL and
IDL cholesterol, higher
triglycerides and
LDL apo B than E 3/3. Overall, the determined
apo B polymorphisms were not related to the slow clearance of autologous
LDL among the 12 patients, in whom autologous
LDL was cleared at a slower rate than homologous
LDL. In conclusion,
hypercholesterolemia can be due to particle-related slow clearance of
LDL in some patients. However, this is not a common cause of
hypercholesterolemia.