Evidence map›Paper›PMID 8163669›Full record

ArticleThe Journal of clinical investigation1994

Overexpression of apolipoprotein CII causes hypertriglyceridemia in transgenic mice.

N S Shachter, T Hayek, T Leff, J D Smith, D W Rosenberg, A Walsh, R Ramakrishnan, I J Goldberg, H N Ginsberg, J L Breslow

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 136 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Quartet of APOCs and the Different Roles They Play in Diabetes.Arteriosclerosis, thrombosis, and vascular biology · 2023
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Age, APOE and sex: Triad of risk of Alzheimer's disease.The Journal of steroid biochemistry and molecular biology · 2016
    Review
  18. Article
  19. Article
  20. Article
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

10 authors at 4 institutions in 2 countries.

N S ShachterLaboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York 10021-6399.
T Hayek
T Leff
J D Smith
D W Rosenberg
A Walsh
R Ramakrishnan
I J Goldberg
H N Ginsberg
J L Breslow
Rockefeller University · USColumbia University · USPfizer (United States) · USRambam Health Care Campus · IL

Funding

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
VITAMIN A TRANSPORT AND RETINOL-BINDING PROTEIN METABOLISMP50HL021006 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI TALL, ALAN RICHARD · 1985 to 1996
–
NHLBI NIH HHS HL-21006NHLBI NIH HHS HL-32435NHLBI NIH HHS HL-33714
6 · The paper itself

Abstract

We have generated transgenic mice expressing the human apolipoprotein CII (apoCII) gene under the transcriptional control of the human cytochrome P-450 IA1 (CYPIA1) promoter. Human apoCII transgenic (HuCIITg) mice exhibited significant basal expression of the transgene (plasma apoCII level = 26.1 +/- 4 mg/dl) and showed further induction of transgene expression after treatment with beta-naphthoflavone. Unexpectedly, HuCIITg mice were hypertriglyceridemic and human apoCII levels correlated strongly to triglyceride levels (R = 0.89, P < 0.0001). Triglyceride levels (mg/dl +/- SEM) were elevated compared to controls in both the fed (804 +/- 113 vs 146 +/- 18, P < 0.001) and fasted (273 +/- 39 vs 61 +/- 4, P < 0.001) states. HuCIITg mice accumulated triglyceride-rich very low density lipoproteins (VLDL) with an increased apoC/apoE ratio. Tracer kinetic studies indicated delayed clearance of VLDL-triglyceride, and studies using Triton inhibition of VLDL clearance showed no increase in VLDL production. Plasma from these mice activated mouse lipoprotein lipase normally and radiolabeled VLDL were normally hydrolyzed. However, HuCIITg VLDL showed markedly decreased binding to heparin-Sepharose, suggesting that apoCII-rich, apoE-poor lipoprotein may be less accessible to cell surface lipases or receptors within their glycosaminoglycan matrices. HuCIITg mice are a promising model of hypertriglyceridemia that suggests a more complex role for apoCII in the metabolism of plasma triglycerides.

Indexed as

AnimalsApolipoprotein C-IIApolipoproteins CBenzoflavonesbeta-NaphthoflavoneCytochrome P-450 Enzyme SystemDisease Models, AnimalFemaleHypertriglyceridemiaLipoprotein LipaseLipoproteins, VLDLMaleMiceMice, Inbred C57BLMice, Inbred DBAMice, TransgenicApolipoprotein C-IIApolipoproteins CBenzoflavonesbeta-NaphthoflavoneCytochrome P-450 Enzyme SystemLipoprotein LipaseLipoproteins, VLDLTriglycerides

Identifiers

PMID8163669
PMCPMC294216
OpenAlexW2022332493

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.