Evidence map›Paper›PMID 24954421›Full record

ArticleJournal of lipid research2014

High density lipoprotein metabolism in low density lipoprotein receptor-deficient mice.

Franz Rinninger, Markus Heine, Roshni Singaraja, Michael Hayden, May Brundert, Rajasekhar Ramakrishnan, Joerg Heeren

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
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  7. The c.*52Biomolecules · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 4 countries.

Franz RinningerDepartment of Medicine, University Hospital Hamburg Eppendorf, 20246 Hamburg, Germany.
Markus HeineDepartment of Biochemistry and Molecular Cell Biology, University Hospital Hamburg Eppendorf, 20246 Hamburg, Germany.
Roshni SingarajaTranslational Laboratories in Genetic Medicine, Agency for Science, Technology and Research National University of Singapore, Singapore 117609 Department of Medicine, National University of Singapore, Singapore 117609.
Michael HaydenCentre for Molecular Medicine and Therapeutics and Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia V5Z 4H4, Canada.
May BrundertDepartment of Medicine, University Hospital Hamburg Eppendorf, 20246 Hamburg, Germany.
Rajasekhar RamakrishnanDepartment of Pediatrics, College of Physicians and Surgeons of Columbia University, New York, NY 10032.
Joerg HeerenDepartment of Biochemistry and Molecular Cell Biology, University Hospital Hamburg Eppendorf, 20246 Hamburg, Germany.
Universität Hamburg · DEAgency for Science, Technology and Research · SGColumbia University · USUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The LDL receptor (LDLR) and scavenger receptor class B type I (SR-BI) play physiological roles in LDL and HDL metabolism in vivo. In this study, we explored HDL metabolism in LDLR-deficient mice in comparison with WT littermates. Murine HDL was radiolabeled in the protein ((125)I) and in the cholesteryl ester (CE) moiety ([(3)H]). The metabolism of (125)I-/[(3)H]HDL was investigated in plasma and in tissues of mice and in murine hepatocytes. In WT mice, liver and adrenals selectively take up HDL-associated CE ([(3)H]). In contrast, in LDLR(-/-) mice, selective HDL CE uptake is significantly reduced in liver and adrenals. In hepatocytes isolated from LDLR(-/-) mice, selective HDL CE uptake is substantially diminished compared with WT liver cells. Hepatic and adrenal protein expression of lipoprotein receptors SR-BI, cluster of differentiation 36 (CD36), and LDL receptor-related protein 1 (LRP1) was analyzed by immunoblots. The respective protein levels were identical both in hepatic and adrenal membranes prepared from WT or from LDLR(-/-) mice. In summary, an LDLR deficiency substantially decreases selective HDL CE uptake by liver and adrenals. This decrease is independent from regulation of receptor proteins like SR-BI, CD36, and LRP1. Thus, LDLR expression has a substantial impact on both HDL and LDL metabolism in mice.

Indexed as

AnimalsATP Binding Cassette Transporter 1Cells, CulturedCholesterol EstersCholesterol, HDLLipid MetabolismLiverMaleMice, Inbred C57BLMice, KnockoutReceptors, LDLTriglyceridesAbca1 protein, mouseATP Binding Cassette Transporter 1Cholesterol EstersCholesterol, HDLReceptors, LDLTriglyceridescholesteryl esterscavenger receptor class B type Iselective uptake

Identifiers

PMID24954421
PMCPMC4617360
OpenAlexW2144234356

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.