On the lipoprotein abnormality in type III hyperlipoproteinemia

Steven Quarfordt; Robert I. Levy; Donald S. Fredrickson

doi:10.1172/JCI106546

On the lipoprotein abnormality in type III hyperlipoproteinemia

Steven Quarfordt, Robert I. Levy, and Donald S. Fredrickson

Published April 1, 1971 - More info

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Abstract

Two lipoprotein species were isolated by starch block electrophoresis from the very low density lipoproteins (VLDL) (S_f 20-400) of patients with type III hyperlipoproteinemia. One of these, α₂-VLDL, had a content of lipid and protein and physical characteristics similar to VLDL from normal subjects or patients with other forms of hyperglyceridemia. The other species, β-VLDL, contained more cholesterol and less triglyceride in relation to the protein, than normal VLDL. Only the apoprotein of low density lipoprotein was immunochemically detectable in the β-VLDL; the proteins in the α₂-VLDL reacted with antisera specific for low density lipoprotein and high density lipoprotein. The electrophoretic mobility of β-VLDL was similar to that of low density lipoprotein and significantly less than that of α₂-VLDL. Isolated β-VLDL had a lesser mean flotation rate than α₂-VLDL, but both α₂- and β-VLDL were found throughout the S_f 20-400 flotation range.

The relative quantities of α₂- and β-VLDL could be varied by changing the diet or by heparin administration. Most of the VLDL from type III patients on a high carbohydrate diet was in the α₂-VLDL form. During fasting, α₂-VLDL fell and β-VLDL increased becoming the predominant species of VLDL. Heparin-induced acceleration of triglyceride clearance also increased β-VLDL and decreased α₂-VLDL. These findings suggest a precursor-product relationship between the α₂- and β-forms of VLDL.

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