Evidence map›Paper›PMID 28217400›Full record

ArticleMetabolomics : Official journal of the Metabolomic Society2016

Novel plasma biomarker of atenolol-induced hyperglycemia identified through a metabolomics-genomics integrative approach.

Felipe A de Oliveira, Mohamed H Shahin, Yan Gong, Caitrin W McDonough, Amber L Beitelshees, John G Gums, Arlene B Chapman, Eric Boerwinkle, Stephen T Turner, Reginald F Frye and 4 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Metabolomics : Official journal of the Metabolomic Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Personalizing treatments for patients based on cardiovascular phenotyping.Expert review of precision medicine and drug development · 2022
    Article
  4. Review
  5. 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

14 authors at 7 institutions in 2 countries.

Felipe A de OliveiraDepartment of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, College of Pharmacy, University of Florida, PO Box 100486, Gainesville, FL 32610-0486, USA.
Mohamed H ShahinDepartment of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, College of Pharmacy, University of Florida, PO Box 100486, Gainesville, FL 32610-0486, USA.
Yan GongDepartment of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, College of Pharmacy, University of Florida, PO Box 100486, Gainesville, FL 32610-0486, USA.
Caitrin W McDonoughDepartment of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, College of Pharmacy, University of Florida, PO Box 100486, Gainesville, FL 32610-0486, USA.
Amber L BeitelsheesDepartment of Medicine, University of Maryland, Baltimore, MD, USA.
John G GumsDepartment of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, College of Pharmacy, University of Florida, PO Box 100486, Gainesville, FL 32610-0486, USA; Department of Community Health and Family Medicine, College of Medicine, University of Florida, Gainesville, FL, USA.
Arlene B ChapmanDepartment of Medicine, University of Chicago, Chicago, IL, USA.
Eric BoerwinkleHuman Genetics Center and Institute for Molecular Medicine, University of Texas Health Science Center, Houston, TX, USA.
Stephen T TurnerCollege of Medicine, Mayo Clinic, Rochester, MN, USA.
Reginald F FryeDepartment of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, College of Pharmacy, University of Florida, PO Box 100486, Gainesville, FL 32610-0486, USA.
Oliver FiehnGenome Center, University of California at Davis, Davis, CA, USA; Biochemistry Department, King Abdullah University, Jeddah, Saudi Arabia.
Rima Kaddurah-DaoukDepartment of Psychiatry and Behavioral Sciences, Duke University, Durham, NC, USA.
Julie A JohnsonDepartment of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, College of Pharmacy, University of Florida, PO Box 100486, Gainesville, FL 32610-0486, USA.
Rhonda M Cooper-DeHoffDepartment of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, College of Pharmacy, University of Florida, PO Box 100486, Gainesville, FL 32610-0486, USA.
University of Florida · USDuke University · USKing Abdulaziz University · SAMayo Clinic · USThe University of Texas Health Science Center at Houston · USUniversity of Chicago · USUniversity of Maryland, Baltimore · US

Funding

Pharmacogenomic Evaluation of Antihypertensive ResponsesU01GM074492 · UNIVERSITY OF FLORIDA · 2005 to 2005
$1.6M
NCATS NIH HHS UL1 TR000064NCATS NIH HHS UL1 TR000135NCATS NIH HHS UL1 TR000454NCATS NIH HHS UL1 TR001427NIGMS NIH HHS RC2 GM092729NIGMS NIH HHS U01 GM074492
6 · The paper itself

Abstract

introductionWhile atenolol is an effective antihypertensive agent, its use is also associated with adverse events including hyperglycemia and incident diabetes that may offset the benefits of blood pressure lowering. By combining metabolomic and genomic data acquired from hypertensive individuals treated with atenolol, it may be possible to better understand the pathways that most impact the development of an adverse glycemic state.

objectiveTo identify biomarkers that can help predict susceptibility to blood glucose excursions during exposure to atenolol.

methodsPlasma samples acquired from 234 Caucasian participants treated with atenolol in the Pharmacogenomic Evaluation of Antihypertensive Responses trial were analyzed by gas chromatography Time-Of-Flight Mass Spectroscopy. Metabolomics and genomics data were integrated by first correlating participant's metabolomic profiles to change in glucose after treatment with atenolol, and then incorporating genotype information from genes involved in metabolite pathways associated with glucose response.

resultsOur findings indicate that the baseline level of β-alanine was associated with glucose change after treatment with atenolol (Q = 0.007, β = 2.97 mg/dL). Analysis of genomic data revealed that carriers of the G allele for SNP rs2669429 in gene

conclusionThese results suggest that β-alanine and rs2669429 may be predictors of atenolol-induced hyperglycemia in Caucasian individuals and further investigation is warranted.

Indexed as

AtenololHyperglycemiaPharmacogenomicsPharmacometabolomicsβ-alanineβ-blockers

Identifiers

PMID28217400
PMCPMC5310671
OpenAlexW2473235487

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.