Submitted on April 24, 2006
Revised on May 22, 2006
Accepted on May 23, 2006
What we have learned about VLDL and LDL metabolism from human kinetic studies
Klaus G. Parhofer and P Hugh R. Barrett
Medical Dpt. II, Grosshadern, Munich 81377
Corresponding Author: Klaus.Parhofer{at}med.uni-muenchen.de
Lipoprotein metabolism is the result of a complex network of many individual components. Abnormal lipoprotein concentrations can result from changes in production, conversion or catabolism of lipoprotein particles. Studies in hypo- and hyperlipoproteinemia have elucidated the processes that control VLDL secretion as well as VLDL and LDL catabolism. In this manuscript we review the current knowledge regarding apoB metabolism focussing on selected clinically relevant conditions. In hypobetalipoproteinemia due to truncations in apoB, the rate of secretion is closely linked to the length of apoB. On the other hand, in patients with the metabolic syndrome it appears that substrate, in the form of free fatty acids, coupled to the state of insulin resistance can induce hypersecretion of VLDL apoB. Studies in patients with familial hypercholesterolemia, familial defective apoB and mutant forms of PCSK9 show that mutations in the LDL receptor, the ligand for the receptor, or an intracellular chaperone for the receptor are the most important determinants in regulating LDL catabolism. This review also demonstrates the variance of results within similar, or even the same, phenotypic conditions. This underscores the sensitivity of metabolic studies to methodological aspects and thus the importance of the inclusion of adequate controls in studies.
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