Evidence map›Paper›PMID 8962133›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1996

Dramatically decreased high density lipoprotein cholesterol, increased remnant clearance, and insulin hypersensitivity in apolipoprotein A-II knockout mice suggest a complex role for apolipoprotein A-II in atherosclerosis susceptibility.

W Weng, J L Breslow

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

45 citing papers in PubMed, 153 citations in OpenAlex.

  1. Context-Dependent Effects of Apolipoprotein A2 on Lipid Metabolism and Atherogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Association between theBiomedicines · 2020
    Article
  10. Generation of Gene-Knockout Mongolian Gerbils via CRISPR/Cas9 System.Frontiers in bioengineering and biotechnology · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. Congenic mice demonstrate the presence of QTLs conferring obesity and hypercholesterolemia on chromosome 1 in the TALLYHO mouse.Mammalian genome : official journal of the International Mammalian Genome Society · 2017
    Article
  15. C57BL/6J mouse apolipoprotein A2 gene is deterministic for apnea.Respiratory physiology & neurobiology · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Cardioprotective functions of HDLs.Journal of lipid research · 2014
    Review
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

2 authors at 1 institution in 1 country.

W WengLaboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York, NY 10021, USA.
J L Breslow
Rockefeller University · US

Funding

Regulation and function of plasma lipid transfer proteinsP01HL054591 · NHLBI · ROCKEFELLER UNIVERSITY · PI GOLDBERG, IRA J · 1995 to 2010
$19.9M
HUMAN DIETARY CHOLESTEROL TOLERANCER01HL032435 · NHLBI · ROCKEFELLER UNIVERSITY · PI BRESLOW, JAN L · 1985 to 2005
$2.5M
ROLE OF APOLIPOPROTEIN GENES IN LIPOPROTEIN METABOLISMR01HL033714 · NHLBI · ROCKEFELLER UNIVERSITY · PI BRESLOW, JAN L · 1985 to 2000
$530k
NHLBI NIH HHS HL32435NHLBI NIH HHS HL33714NHLBI NIH HHS HL54591NHLBI NIH HHS P01 HL054591NHLBI NIH HHS R01 HL032435
6 · The paper itself

Abstract

Apolipoprotein (apo) A-II is the second most abundant apolipoprotein in high density lipoprotein (HDL). To study its role in lipoprotein metabolism and atherosclerosis susceptibility, apo A-II knockout mice were created. Homozygous knockout mice had 67% and 52% reductions in HDL cholesterol levels in the fasted and fed states, respectively, and HDL particle size was reduced. Metabolic turnover studies revealed the HDL decrease to be due to both decreased HDL cholesterol ester and apo A-I transport rate and increased HDL cholesterol ester and apo A-I fractional catabolic rate. The apo A-II deficiency trait was bred onto the atherosclerosis-prone apo E-deficient background, which resulted in a surprising 66% decrease in cholesterol levels due primarily to decreased atherogenic lipoprotein remnant particles. Metabolic turnover studies indicated increased remnant clearance in the absence of apo A-II. Finally, apo A-II deficiency was associated with lower free fatty acid, glucose, and insulin levels, suggesting an insulin hypersensitivity state. In summary, apo A-II plays a complex role in lipoprotein metabolism, with some antiatherogenic properties such as the maintenance of a stable HDL pool, and other proatherogenic properties such as decreasing clearance of atherogenic lipoprotein remnants and promotion of insulin resistance.

Indexed as

AnimalsApolipoprotein A-IIArteriosclerosisCholesterol, HDLGenetic Predisposition to DiseaseInsulinMiceMice, KnockoutApolipoprotein A-IICholesterol, HDLInsulin

Identifiers

PMID8962133
PMCPMC26214
OpenAlexW2103648242

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.