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Accumulation of an apoE-poor subfraction of very low density lipoprotein in hypertriglyceridemic men.
J Lipid Res. 1989 Nov; 30(11):1691-701.JL

Abstract

Studies were undertaken to investigate the mechanism of the marked accumulation of an apoE-poor very low density lipoprotein (VLDL) subfraction in untreated Type IV and IIb hypertriglyceridemic subjects. Heparin-Sepharose chromatography was used to separate large VLDL (Sf 60-400) from fasted subjects, into an apoE-poor, unbound fraction and an apoE-rich, bound fraction. As a percent of total VLDL protein, the apoE-poor fraction comprised 40 +/- 4% of total VLDL in hypertriglyceridemic subjects versus 25% in normal subjects. Compared to the apoE-rich, bound fraction, this apoE-poor material was found to have a 5-fold lower ratio of apoE to apoC (0.20 +/- 0.06 vs 0.91 +/- 0.18, P less than 0.005), but a 1.5-fold higher ratio of triglyceride to protein (11.41 +/- 0.85 vs 7.97 +/- 0.77, P less than 0.01). In addition, the apoE-poor fraction was found to be enriched 2-fold in apoB-48 (10.30 +/- 2.41% vs 5.73 +/- 1.59% of total apoB, P less than 0.005) compared to the apoE-rich fraction, suggesting that the apoE-poor fraction contains more chylomicron remnants. The amount of this apoE-poor VLDL was markedly reduced following a reduction in VLDL triglyceride levels (a decrease from 40 +/- 4% to 21 +/- 2% of VLDL protein following a 50% reduction in VLDL triglyceride levels). The large VLDL from Type I, III, and V hyperlipoproteinemic subjects subfractionated using heparin-Sepharose showed an equal distribution of apoE between the two fractions in contrast with the Type IV and IIb subjects. The separation of VLDL from Type I, III, and V subjects using heparin-Sepharose involves a mechanism other than apoE binding. Separation in the latter likely results from apoB-100 binding to heparin, as opposed to apoE binding of VLDL from Type IV and IIb subjects.

Authors+Show Affiliations

Department of Medicine, University of Western Ontario, London, Canada.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

2614271

Citation

Evans, A J., et al. "Accumulation of an apoE-poor Subfraction of Very Low Density Lipoprotein in Hypertriglyceridemic Men." Journal of Lipid Research, vol. 30, no. 11, 1989, pp. 1691-701.
Evans AJ, Huff MW, Wolfe BM. Accumulation of an apoE-poor subfraction of very low density lipoprotein in hypertriglyceridemic men. J Lipid Res. 1989;30(11):1691-701.
Evans, A. J., Huff, M. W., & Wolfe, B. M. (1989). Accumulation of an apoE-poor subfraction of very low density lipoprotein in hypertriglyceridemic men. Journal of Lipid Research, 30(11), 1691-701.
Evans AJ, Huff MW, Wolfe BM. Accumulation of an apoE-poor Subfraction of Very Low Density Lipoprotein in Hypertriglyceridemic Men. J Lipid Res. 1989;30(11):1691-701. PubMed PMID: 2614271.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Accumulation of an apoE-poor subfraction of very low density lipoprotein in hypertriglyceridemic men. AU - Evans,A J, AU - Huff,M W, AU - Wolfe,B M, PY - 1989/11/1/pubmed PY - 1989/11/1/medline PY - 1989/11/1/entrez SP - 1691 EP - 701 JF - Journal of lipid research JO - J Lipid Res VL - 30 IS - 11 N2 - Studies were undertaken to investigate the mechanism of the marked accumulation of an apoE-poor very low density lipoprotein (VLDL) subfraction in untreated Type IV and IIb hypertriglyceridemic subjects. Heparin-Sepharose chromatography was used to separate large VLDL (Sf 60-400) from fasted subjects, into an apoE-poor, unbound fraction and an apoE-rich, bound fraction. As a percent of total VLDL protein, the apoE-poor fraction comprised 40 +/- 4% of total VLDL in hypertriglyceridemic subjects versus 25% in normal subjects. Compared to the apoE-rich, bound fraction, this apoE-poor material was found to have a 5-fold lower ratio of apoE to apoC (0.20 +/- 0.06 vs 0.91 +/- 0.18, P less than 0.005), but a 1.5-fold higher ratio of triglyceride to protein (11.41 +/- 0.85 vs 7.97 +/- 0.77, P less than 0.01). In addition, the apoE-poor fraction was found to be enriched 2-fold in apoB-48 (10.30 +/- 2.41% vs 5.73 +/- 1.59% of total apoB, P less than 0.005) compared to the apoE-rich fraction, suggesting that the apoE-poor fraction contains more chylomicron remnants. The amount of this apoE-poor VLDL was markedly reduced following a reduction in VLDL triglyceride levels (a decrease from 40 +/- 4% to 21 +/- 2% of VLDL protein following a 50% reduction in VLDL triglyceride levels). The large VLDL from Type I, III, and V hyperlipoproteinemic subjects subfractionated using heparin-Sepharose showed an equal distribution of apoE between the two fractions in contrast with the Type IV and IIb subjects. The separation of VLDL from Type I, III, and V subjects using heparin-Sepharose involves a mechanism other than apoE binding. Separation in the latter likely results from apoB-100 binding to heparin, as opposed to apoE binding of VLDL from Type IV and IIb subjects. SN - 0022-2275 UR - https://www.unboundmedicine.com/medline/citation/2614271/Accumulation_of_an_apoE_poor_subfraction_of_very_low_density_lipoprotein_in_hypertriglyceridemic_men_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2275(20)38218-3 DB - PRIME DP - Unbound Medicine ER -