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Rapid Publication Free access | 10.1172/JCI108999

Catabolism of Very Low Density Lipoprotein B Apoprotein in Man

Michael F. Reardon, Noel H. Fidge, and Paul J. Nestel

Department of Clinical Science, John Curtin School of Medicial Research, Australian National University, Canberra A.C.T. 2600

Cardiovascular Metabolism and Nutrition Research Unit, Baker Medical Research Institute, Melbourne, Victoria 3181, Australia

Find articles by Reardon, M. in: PubMed | Google Scholar

Department of Clinical Science, John Curtin School of Medicial Research, Australian National University, Canberra A.C.T. 2600

Cardiovascular Metabolism and Nutrition Research Unit, Baker Medical Research Institute, Melbourne, Victoria 3181, Australia

Find articles by Fidge, N. in: PubMed | Google Scholar

Department of Clinical Science, John Curtin School of Medicial Research, Australian National University, Canberra A.C.T. 2600

Cardiovascular Metabolism and Nutrition Research Unit, Baker Medical Research Institute, Melbourne, Victoria 3181, Australia

Find articles by Nestel, P. in: PubMed | Google Scholar

Published March 1, 1978 - More info

Published in Volume 61, Issue 3 on March 1, 1978
J Clin Invest. 1978;61(3):850–860. https://doi.org/10.1172/JCI108999.
© 1978 The American Society for Clinical Investigation
Published March 1, 1978 - Version history
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Abstract

The turnover and the catabolic fate of the B apoprotein of very low density lipoprotein (VLDL-B) was studied in 15 normal and hyperlipidemic subjects using reinjected autologous VLDL labeled with radioiodine. The specific radioactivity-time curve of the B apoprotein in total VLDL (Sf20-400) was multiexponential but conformed to a two-pool model during the first 48 h of catabolism. The flux was highest in several hypertriglyceridemic subjects. The mass of pool A exceeded the intravascular content of VLDL-B by 30% on average, indicating extravascular metabolism of VLDL. The two-pool model might reflect the input of several populations of particles or heterogeneity of catabolic processes or pools. The flux of B apoprotein was also measured in several subclasses of VLDL, in smaller intermediate density lipoproteins, and in low density lipoproteins (LDL). In three subjects the flux was similar in Sf 60-400 and in Sf 12-60 lipoproteins, suggesting that VLDL was catabolized at least to a particle in the density range Sf 12-60. Subsequent catabolism appeared to proceed by two pathways: in normotriglyceridemic subjects, B apoprotein flux in the Sf 20-400 and in Sf 12-20 lipoproteins was similar, whereas in hypertriglyceridemic subjects flux through Sf 12-20 accounted for only part of the VLDL-B flux.

The flux of low density lipoprotein B apoprotein (LDL-B), which is believed to be derived from VLDL catabolism, was calculated from the area between the specific activity time curves of VLDL-B and LDL-B. In subjects with normal plasma triglyceride concentration, LDL-B flux was from 91% to 113% of that of VLDL-B; but in three hypertriglyceridemic subjects showing high rates of VLDL-B transport, LDL-B flux was only one-third that of VLDL-B. This suggests that when VLDL-B flux is high, VLDL is substantially catabolized by a route other than through LDL and possibly leaves the circulation as a particle in the Sf 20-60 density range.

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