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Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation.

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Linton, M F, Gish, R, Hubl, S T, Bütler, E, Esquivel, C, Bry, W I, Boyles, J K, Wardell, M R +1 more·1991·Journal of Clinical Investigation
DOI 10.1172/jci115288
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Abstract

Apolipoprotein (apo) E and the two B apolipoproteins, apoB48 and apoB100, are important proteins in human lipoprotein metabolism. Commonly occurring polymorphisms in the genes for apoE and apoB result in amino acid substitutions that produce readily detectable phenotypic differences in these proteins. We studied changes in apoE and apoB phenotypes before and after liver transplantation to gain new insights into apolipoprotein physiology. In all 29 patients that we studied, the postoperative serum apoE phenotype of the recipient, as assessed by isoelectric focusing, converted virtually completely to that of the donor, providing evidence that greater than 90% of the apoE in the plasma is synthesized by the liver. In contrast, the cerebrospinal fluid apoE phenotype did not change to the donor's phenotype after liver transplantation, indicating that most of the apoE in CSF cannot be derived from the plasma pool and therefore must be synthesized locally. The apoB100 phenotype (assessed with immunoassays using monoclonal antibody MB19, an antibody that detects a two-allele polymorphism in apoB) invariably converted to the phenotype of the donor. In four normolipidemic patients, we determined the MB19 phenotype of both the apoB100 and apoB48 in the "chylomicron fraction" isolated from plasma 3 h after a fat-rich meal. Interestingly, the apoB100 in the chylomicron fraction invariably had the phenotype of the donor, indicating that the vast majority of the large, triglyceride-rich apoB100-containing lipoproteins that appear in the plasma after a fat-rich meal are actually VLDL of hepatic origin. The MB19 phenotype of the apoB48 in the plasma chylomicron fraction did not change after liver transplantation, indicating that almost all of the apoB48 in plasma chylomicrons is derived from the intestine. These results were consistent with our immunocytochemical studies on intestinal biopsy specimens of organ donors; using apoB-specific monoclonal antibodies, we found evidence for apoB48, but not apoB100, in donor intestinal biopsy specimens.

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  • ApoE in the periphery and the central nervous system are independent of each other and produced from different sources.

    “ApoE found in the periphery and the central nervous system (CNS) are independent of each other and produced from different sources [3].”

    From In Vivo Human Apolipoprotein E Isoform Fractional Turnover Rates in the CNS (2012) · cites this paper as [3]

    The Results report that serum apoE largely reflects the donor liver after transplantation, while CSF apoE retains the recipient phenotype, implying that most CSF apoE is produced locally. This supports different predominant sources, but not the unqualified claim that peripheral and CNS apoE are entirely independent. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Limited blood-brain barrier permeability to circulating lipid-poor apoE2, apoE3, and apoE4 supports that apoE in blood and brain are regulated independently.

    “A limited blood brain barrier permeability to circulating lipidpoor apoE2, apoE3, and apoE4 supports that apoE in blood and brain are regulated independently [72,107,108].”

    From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [72]

    The Results (page not provided) report that serum apoE phenotypes changed after liver transplantation while CSF phenotypes did not, implying that most CSF apoE is produced locally. This supports largely separate blood and brain apoE pools, but the paper does not test blood-brain barrier permeability specifically for circulating lipid-poor apoE2, apoE3, and apoE4. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • ApoE in the brain and CSF is synthesized within the central nervous system and is not derived from other organs.

    “ApoE in the brain and CSF is synthesized within the central nervous system and is not derived from other organs.13”

    From ApoE is Secreted as a Lipid Nanoparticle by Mammalian Cells: Implications for Alzheimer’s Disease Pathogenesis (2025) · cites this paper as [13]

    The Results report that brain astrocytes synthesize apoE and that the unchanged CSF apoE phenotype after liver transplantation implies most CSF apoE is produced locally. The paper says “most” or “the majority,” not that all apoE in the brain and CSF is synthesized within the CNS or that none is derived from other organs. Page numbers were not provided in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • APOE circulating in the blood is predominantly produced by the liver; however, the BBB keeps this pool of peripheral APOE separated from that produced in the CNS.

    “APOE circulating in the blood is predominantly produced by the liver; however, the BBB keeps this pool of peripheral APOE separated from that produced in the CNS181,182.”

    From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [182]

    The Results report that at least 90% of serum apoE is synthesized by the liver. They also report that CSF apoE retained the recipient’s phenotype after liver transplantation, implying that most CSF apoE is produced locally. The paper does not establish that the blood–brain barrier keeps the two pools wholly separate; it considers entry from plasma as a possible source of CSF apoE. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • ApoE in blood and brain are regulated independently.

    “suggesting that apoE in blood and brain are regulated independently.61,63”

    From Plasma levels of apolipoprotein E, <i>APOE</i> genotype, and all-cause and cause-specific mortality in 105 949 individuals from a white general population cohort (2019) · cites this paper as [61]

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1 of the 60 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Butler, R. 1990. Advances in Forensic Science. Vol. 3. DNA and Other Polymorphisms in Forensic Sciences.

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Authors
Linton, M. F., Gish, R., Hubl, S. T., Bütler, E., Esquivel, C., Bry, W. I., Boyles, J. K., Wardell, M. R., & Young, S. G.
Affiliations
  • University of California, San Francisco (US)
  • Gladstone Institutes (US)
ORCID
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1991-07-01
Volume
88
Issue
1
Pages
270-281
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci115288
OpenAlex
W2115309238
Cited by
367
References
60
Citations by year
2026: 8 · 2025: 20 · 2024: 12 · 2023: 20 · 2022: 18 · 2021: 11 · 2020: 25 · 2019: 13 · 2018: 4 · 2017: 9 · 2016: 8 · 2015: 11 · 2014: 13 · 2013: 10 · 2012: 11
FWCI
4.40
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Heart Association
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (HL-41633, P01HL041633, HL 01672)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
Keywords
apolipoprotein E, apolipoprotein B, apolipoprotein B-48, apolipoprotein B-100, liver transplantation, chylomicrons, VLDL, lipoprotein metabolism
MeSH terms
Adult, Apolipoproteins B, Apolipoproteins E, Chylomicrons, Glycosylation, Humans, Immunohistochemistry, Lipoproteins, VLDL, Middle Aged, Phenotype, Liver Transplantation

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