Evidence map›Paper›PMID 27106679›Full record

ArticleObesity (Silver Spring, Md.)2016

Proinflammatory and lipid biomarkers mediate metabolically healthy obesity: A proteomics study.

Ayo Priscille Doumatey, Jie Zhou, Ming Zhou, DaRue Prieto, Charles N Rotimi, Adebowale Adeyemo

Open access · hybridAbstract read
In one paragraph

Article in Obesity (Silver Spring, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 15% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Ayo Priscille DoumateyCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA.
Jie ZhouCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA.
Ming ZhouLaboratory of Proteomics and Analytical Technologies (LPAT) Leidos Biomedical Research Inc, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA.
DaRue PrietoLaboratory of Proteomics and Analytical Technologies (LPAT) Leidos Biomedical Research Inc, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA.
Charles N RotimiCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA.
Adebowale AdeyemoCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA.
National Institutes of Health · USNational Cancer Institute · US

Funding

Genetic epidemiology of complex diseasesZIAHG200362 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI ROTIMI, CHARLES · 2009 to 2025
$54.7M
Genetic epidemiology of complex diseasesZ01HG200362 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI ROTIMI, CHARLES · 2008 to 2008
$1.7M
MINORITY INTERNATIONAL RESEARCH TRAINING GRANTT37TW000041 · FIC · HOWARD UNIVERSITY · PI ADAMS-CAMPBELL, LUCILE L · 1993 to 1998
–
FIC NIH HHS T37 TW000041Intramural NIH HHS Z99 HG999999NHGRI NIH HHS Z01 HG200362
6 · The paper itself

Abstract

objectiveThe metabolically healthy obesity (MHO) phenotype is an important obesity subtype in which obesity is not accompanied by any metabolic comorbidity. However, the underlying molecular mechanisms remain elusive. In this study, a shotgun proteomics approach to identify circulating biomolecules and pathways associated with MHO was used.

methodsThe subjects were 20 African-American women: 10 MHO cases and 10 metabolically abnormal individuals with obesity (MAO) controls. Serum proteins were detected and quantified using label-free proteomics. Differential expression of proteins between the two groups was analyzed, and the list of differentially expressed proteins was analyzed to determine enriched biological pathways.

resultsTwenty proteins were differentially expressed between MHO and controls. These proteins included: hemoglobin subunits (HBA1, P = 6.00 × 10(-18) ), haptoglobin-related protein (HPR, P = 1.2 × 10(-15) ), apolipoproteins (APOB-100, P = 1.50 × 10(-40) ; APOA4, P = 1.1 × 10(-14) ), retinol-binding protein 4 (RBP4, P = 7.1 × 10(-08) ), and CRP (P = 2.0 × 10(-04) ). MHO was associated with lower levels of proinflammatory and higher levels of anti-inflammatory biomarkers when compared with MAO. Pathway analysis showed enrichment of lipids and inflammatory pathways, including LXR/RXR and FXR/RXR activation, and acute phase response signaling.

conclusionsThese findings suggested that protection from dysregulated inflammatory and lipid processes were primary molecular hallmarks of MHO. The candidate biomarkers (AHSG, RBP4, and APOA4) identified in this study are potential prognostic markers for MHO.

Indexed as

AdultApolipoprotein B-100BiomarkersBlack or African AmericanBody Mass IndexCase-Control StudiesFemaleHomocysteineHumansInflammationLipidsMaleMiddle AgedObesityObesity, Metabolically BenignPhenotypeAPOB protein, humanApolipoprotein B-100BiomarkersHomocysteineLipids

Identifiers

PMID27106679
PMCPMC4882259
OpenAlexW2340431754

What OpenQuestion holds

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Registered trials

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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.