Evidence map›Paper›PMID 16822320›Full record

ArticleLipids in health and disease2006

The lipoprotein lipase gene in combined hyperlipidemia: evidence of a protective allele depletion.

Shu-Fen Wung, Medha V Kulkarni, Clive R Pullinger, Mary J Malloy, John P Kane, Bradley E Aouizerat

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2006. 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
1.4field-weighted citation impact, top 17% 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, 23 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Lipoprotein lipase gene Hind III polymorphism was associated with hemorrhagic stroke.International journal of clinical and experimental medicine · 2015
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Galanin preproprotein is associated with elevated plasma triglycerides.Arteriosclerosis, thrombosis, and vascular biology · 2009
    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

6 authors at 3 institutions in 1 country.

Shu-Fen WungCollege of Nursing, University of Arizona, Tucson, AZ, USA. shufen@nursing.arizona.edu
Medha V Kulkarni
Clive R Pullinger
Mary J Malloy
John P Kane
Bradley E Aouizerat
University of California, San Francisco · USCenter for Human Genetics · USUniversity of Arizona · US

Funding

ANTIATHEROGENIC EFFECTS OF MODERATE ALCOHOL USER01AA011205 · NIAAA · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI MALLOY, MARY J · 1996 to 2000
$223k
DETERMINENTS OF CORONARY DISEASER01HL050779 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI MALLOY, MARY J · 1994 to 1997
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SPECIATION OF HDL AND LDLR01HL050782 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI KANE, JOHN P · 1994 to 1997
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NHLBI NIH HHS HL50779NHLBI NIH HHS HL50782NIAAA NIH HHS AA11205
6 · The paper itself

Abstract

backgroundLipoprotein Lipase (LPL), a key enzyme in lipid metabolism, catalyzes the hydrolysis of triglycerides (TG) from TG-rich lipoproteins, and serves a bridging function that enhances the cellular uptake of lipoproteins. Abnormalities in LPL function are associated with pathophysiological conditions, including familial combined hyperlipidemia (FCH). Whereas two LPL susceptibility alleles were found to co-segregate in a few FCH kindred, a role for common, protective alleles remains unexplored. The LPL Ser447Stop (S447X) allele is associated with anti-atherogenic lipid profiles and a modest reduction in risk for coronary disease. We hypothesize that significant depletion of the 447X allele exists in combined hyperlipidemia cases versus controls. A case-control design was employed. The polymorphism was assessed by restriction assay in 212 cases and 161 controls. Genotypic, allelic, and phenotypic associations were examined.

resultsWe found evidence of significant allelic (447Xcontrol: 0.130 vs. 447Xcase: 0.031, chi2 = 29.085; 1df; p < 0.001) and genotypic association (SS: 0.745 vs. 0.939, and SX+XX: 0.255 vs. 0.061) in controls and cases, respectively (chi2 = 26.09; 1df; p < 0.001). In cases, depletion of the 447X allele is associated with a significant elevation in very-low-density lipoprotein cholesterol (VLDL-C, p = 0.045). Consonant with previous studies of this polymorphism, regression models predict that carriers of the 447X allele displayed significantly lower TG, low-density lipoprotein cholesterol (LDL-C) and TG/high-density lipoprotein cholesterol (HDL-C) ratio.

conclusionThese findings suggest a role for the S447X polymorphism in combined hyperlipidemia and demonstrate the importance of evaluating both susceptibility and protective genetic risk factors.

Indexed as

Gene DeletionAdultAgedAllelesFemaleHumansHyperlipidemia, Familial CombinedLipoprotein LipaseLipoproteinsMaleMiddle AgedPolymorphism, Single NucleotideLipoprotein LipaseLipoproteins

Identifiers

PMID16822320
PMCPMC1538992
OpenAlexW2099222826

What OpenQuestion holds

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LicenceCC BY
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.