Evidence map›Paper›PMID 19656007›Full record

ArticleMetabolic syndrome and related disorders2009

Genetic variants of the ENPP1/PC-1 gene are associated with hypertriglyceridemia in male subjects.

Sinan Tanyolaç, Andrew A Bremer, Uğur Hodoglugil, Irina Movsesyan, Clive R Pullinger, Steven W Heiner, Mary J Malloy, John P Kane, Ira D Goldfine

Abstract read
In one paragraph

Article in Metabolic syndrome and related disorders, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

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2 · The registry

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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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The genetics of human obesity.Annals of the New York Academy of Sciences · 2013
    Review
  7. New Insights into the Role of ENPP1 in Insulin Resistance.Journal of metabonomics & metabolites · 2012
    Article
  8. Article
4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Sinan TanyolaçDiabetes Center and Department of Medicine, University of California, San Francisco, California 94115, USA.
Andrew A Bremer
Uğur Hodoglugil
Irina Movsesyan
Clive R Pullinger
Steven W Heiner
Mary J Malloy
John P Kane
Ira D Goldfine
University of California, San Francisco · USBrigham Young University · USGladstone Institutes · USUniversity of California Davis Medical Center · US

Funding

PC-1 Insulin Receptor SignalingR01DK056933 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GOLDFINE, IRA D. · 2001 to 2009
$2.6M
NIDDK NIH HHS DK056933
6 · The paper itself

Abstract

backgroundHypertriglyceridemia is associated with insulin resistance, type 2 diabetes, and the metabolic syndrome. Membrane glycoprotein PC-1 (also termed ENPP1) is a direct insulin receptor inhibitor, and certain polymorphisms of the ENPP1/PC-1 gene have been associated with insulin resistance, type 2 diabetes, obesity, and diabetic complications.

methodsWe examined the effect of 3 ENPP1/PC-1 variants (K121Q, rs1044498, and IVS20delT-11, rs1799774, and A-->G+1044TGA, rs7754561) on plasma triglyceride levels in 1112 subjects of non-Hispanic American white European ancestry.

resultsTwo of the ENPP1/PC-1 variants--A-->G+1044TGA (odds ratio [OR] 1.48, 95% confidence interval [CI], 1.54-1.82, P = 0.002) and IVS20delT-11 (OR 1.41, 95% CI, 1.08-1.84, P = 0.012)--were significantly associated with hypertriglyceridemia. Haplotype analyses also revealed an association with hypertriglyceridemia. In the variant analyses and in the haplotype analysis, the associations with hypertriglyceridemia were observed in male but not female subjects. Interestingly, the more widely studied K121Q ENPP1/PC-1 variant was not associated with hypertriglyceridemia in any group or subgroup analysis.

conclusionIn the present study, we find that genetic variants of the ENPP1/PC-1 gene are associated with hypertriglyceridemia in male subjects, and may contribute to the development of the insulin resistance/metabolic syndrome in this population.

Indexed as

Genetic Variation3' Untranslated RegionsAmino Acid SubstitutionCase-Control StudiesDiabetes Mellitus, Type 2EuropeFemaleGene FrequencyHaplotypesHumansHypertriglyceridemiaIntronsMaleMiddle AgedPhosphoric Diester HydrolasesPolymorphism, Single Nucleotide3' Untranslated Regionsectonucleotide pyrophosphatase phosphodiesterase 1Phosphoric Diester HydrolasesPyrophosphatases

Identifiers

PMID19656007
PMCPMC3139525
OpenAlexW1974904414

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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.