Evidence map›Paper›PMID 10725355›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Apolipoprotein E regulates dietary cholesterol absorption and biliary cholesterol excretion: studies in C57BL/6 apolipoprotein E knockout mice.

E Sehayek, S Shefer, L B Nguyen, J G Ono, M Merkel, J L Breslow

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Neuronal ApoE Regulates the Cell-to-Cell Transmission of α-Synuclein.International journal of molecular sciences · 2022
    Article
  6. Review
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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

6 authors at 1 institution in 1 country.

E SehayekLaboratory of Biochemical Genetics and Metabolism, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.
S Shefer
L B Nguyen
J G Ono
M Merkel
J L Breslow
Rockefeller University · US

Funding

HUMAN DIETARY CHOLESTEROL TOLERANCER01HL032435 · NHLBI · ROCKEFELLER UNIVERSITY · PI BRESLOW, JAN L · 1985 to 2005
$2.5M
INBORN ERRORS IN BILE ACID SYNTHESISR01DK026756 · NIDDK · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SHEFER, SARAH · 1986 to 2000
$476k
INBORN ERRORS IN BILE ACID SYNTHESISR37DK026756 · NIDDK · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SHEFER, SARAH · 1989 to 1996
–
NHLBI NIH HHS HL-32435-14NHLBI NIH HHS R01 HL032435NIDDK NIH HHS DK 26756
6 · The paper itself

Abstract

The present study examined the role of apolipoprotein E (apoE) in the regulation of dietary cholesterol absorption and biliary cholesterol excretion. Increasing dietary cholesterol from 0.02% to 0.5% in C57BL/6 wild-type mice decreased the percentage of dietary cholesterol that is absorbed by 25%, and this decrease was associated with a 2-fold increase in gallbladder biliary cholesterol concentration. In contrast, increasing dietary cholesterol from 0. 02% to 0.5% in C57BL/6 apoE knockout mice produced no significant suppression of the percentage dietary cholesterol absorption and increased gallbladder biliary cholesterol concentration only 16%. Whereas in wild-type mice, the increase in dietary cholesterol increased the hepatic excretion of biliary cholesterol 4-fold, there was only a 2-fold increase in apoE knockout mice. On both the low- and the high-cholesterol diets, whole liver and isolated hepatocyte cholesterol content was higher in the apoE knockout mice. These results suggest that, in response to dietary cholesterol, apoE may play a critical role in decreasing the percentage absorption of dietary cholesterol and increasing biliary cholesterol excretion. These observations suggest a mechanism whereby the absence of apoE contributes to the propensity for tissue cholesterol deposition and accelerated atherogenesis in apoE knockout mice.

Indexed as

AnimalsApolipoproteins ECholesterolCholesterol, DietaryGallbladderLiverMiceMice, Inbred C57BLMice, KnockoutApolipoproteins ECholesterolCholesterol, Dietary

Identifiers

PMID10725355
PMCPMC16257
OpenAlexW2059977095

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.