Evidence map›Paper›PMID 8698877›Full record

ArticleThe Journal of clinical investigation1996

Combined hyperlipidemia in transgenic mice overexpressing human apolipoprotein Cl.

N S Shachter, T Ebara, R Ramakrishnan, G Steiner, J L Breslow, H N Ginsberg, J D Smith

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Quartet of APOCs and the Different Roles They Play in Diabetes.Arteriosclerosis, thrombosis, and vascular biology · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Apolipoprotein C1: Its Pleiotropic Effects in Lipid Metabolism and Beyond.International journal of molecular sciences · 2019
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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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 3 institutions in 2 countries.

N S ShachterDepartment of Medicine, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA. nss5@columbia.edu
T Ebara
R Ramakrishnan
G Steiner
J L Breslow
H N Ginsberg
J D Smith
Columbia University · USRockefeller University · USUniversity of Toronto · CA

Funding

VITAMIN A TRANSPORT AND RETINOL-BINDING PROTEIN METABOLISMP50HL021006 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI TALL, ALAN RICHARD · 1985 to 1996
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REGULATION OF APOPROTEIN-B METABOLISM IN HUMANSR01HL036000 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI GINSBERG, HENRY N · 1985 to 1995
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NHLBI NIH HHS HL-21006NHLBI NIH HHS HL-36000
6 · The paper itself

Abstract

We have generated transgenic mice over-expressing human apolipoprotein CI (apo CI) using the native gene joined to the downstream 154-bp liver-specific enhancer that we defined for apo E. Human apo CI (HuCI)-transgenic mice showed elevation of plasma triglycerides (mg/dl) compared to controls in both the fasted (211 +/- 81 vs 123 +/- 52, P = 0.0001) and fed (265 +/- 105 vs 146 +/- 68, P < 0.0001) states. Unlike the human apo CII (HuCII)- and apo CIII (HuCIII)-transgenic mouse models of hypertriglyceridemia, plasma cholesterol was disproportionately elevated (95 +/- 23 vs 73 +/- 23, P = 0.002, fasted and 90 +/- 24 vs 61 +/- 14, P < 0.0001, fed). Lipoprotein fractionation showed increased VLDL and IDL + LDL with an increased cholesterol/triglyceride ratio (0.114 vs 0.065, P = 0.02, in VLDL). The VLDL apo E/apo B ratio was decreased 3.4-fold (P = 0.05) and apo CII and apo CIII decreased in proportion to apo E. Triglyceride and apo B production rates were normal, but clearance rates of VLDL triglycerides and postlipolysis lipoprotein "remnants" were significantly slowed. Plasma apo B was significantly elevated. Unlike HuCII- and HuCIII-transgenic mice, VLDL from HuCI transgenic mice bound heparin-Sepharose, a model for cell-surface glycosaminoglycans, normally. In summary, apo CI overexpression is associated with decreased particulate uptake of apo B-containing lipoproteins, leading to increased levels of several potentially atherogenic species, including cholesterol-enriched VLDL, IDL, and LDL.

Indexed as

AnimalsApolipoprotein C-IApolipoproteins BApolipoproteins CCholesterolFemaleHumansHyperlipidemiasLipoproteinsLipoproteins, VLDLMaleMiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicApolipoprotein C-IApolipoproteins BApolipoproteins CCholesterolLipoproteinsLipoproteins, VLDL

Identifiers

PMID8698877
PMCPMC507495
OpenAlexW2031053394

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.