Evidence map›Paper›PMID 1918380›Full record

ArticleThe Journal of clinical investigation1991

Lipoprotein lipase modulates net secretory output of apolipoprotein B in vitro. A possible pathophysiologic explanation for familial combined hyperlipidemia.

K J Williams, K A Petrie, R W Brocia, T L Swenson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

12 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Presecretory oxidation, aggregation, and autophagic destruction of apoprotein-B: a pathway for late-stage quality control.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Physical activity and lipoprotein lipid disorders.Sports medicine (Auckland, N.Z.) · 1994
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

4 authors at 2 institutions in 1 country.

K J WilliamsDepartment of Physiology and Biochemistry, Medical College of Pennsylvania, Philadelphia 19129.
K A Petrie
R W Brocia
T L Swenson
Merck & Co., Inc., Rahway, NJ, USA (United States) · USDrexel University · US

Funding

LIPOPROTEIN LIPASE AND ATHEROGENESISR01HL038956 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI WILLIAMS, KEVIN JON · 1994 to 1998
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METABOLISM OF A SYNTHETIC ANTI-ATHEROGENIC LIPOPROTEINR29HL038956 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI WILLIAMS, KEVIN JON · 1987 to 1991
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NHLBI NIH HHS HL-38956
6 · The paper itself

Abstract

We showed previously that net secretory output of apolipoprotein B (apo B) from cultured human hepatoma cells (HepG2) is regulated by rapid reuptake of nascent lipoproteins before they have diffused away from the vicinity of the cells. We now sought to determine if the nascent lipoproteins could be remodeled to enhance or impede reuptake. We found that lipoprotein lipase (LpL), an enzyme that hydrolyzes lipoprotein triglyceride, reduced HepG2 output of apo B to one-quarter to one-half of control. The reduction was apparent during co-incubations as short as 2 h and as long as 24 h. Heparin, which blocks receptor-mediated binding of lipoproteins, abolished the effect of LpL on apo B output, without causing enzyme inhibition. To assess uptake directly, we prepared labeled nascent lipoproteins. LpL tripled the cellular uptake of labeled nascent lipoproteins, from 15.2% +/- 0.7% to 48.7% +/- 0.3% of the total applied to the cells. Cellular uptake of 125I-labeled anti-LDL receptor IgG was unaffected by LpL; thus, LpL enhanced reuptake by altering lipoproteins, not receptors. Because LpL is present in the space of Disse in the liver, we conclude that LpL may act on newly secreted lipoproteins to enhance reuptake in vivo. LpL deficiency would reduce local reuptake of apo B, which would appear as overproduction, thereby providing a mechanistic link between partial LpL deficiency and familial combined hyperlipidemia.

Indexed as

Apolipoproteins BCell LineHumansHyperlipidemia, Familial CombinedLipoprotein LipaseLipoproteins, LDLReceptors, LDLApolipoproteins BLipoprotein LipaseLipoproteins, LDLReceptors, LDL

Identifiers

PMID1918380
PMCPMC295599
OpenAlexW2004282447

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.