Evidence map›Paper›PMID 24901842›Full record

ArticlePloS one2014

Body fat percentage is a major determinant of total bilirubin independently of UGT1A1*28 polymorphism in young obese.

Luís Belo, Henrique Nascimento, Michaela Kohlova, Elsa Bronze-da-Rocha, João Fernandes, Elísio Costa, Cristina Catarino, Luísa Aires, Helena Ferreira Mansilha, Petronila Rocha-Pereira and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

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  13. Biliverdin reductase and bilirubin in hepatic disease.American journal of physiology. Gastrointestinal and liver physiology · 2018
    Review
  14. Bilirubin in the Liver-Gut Signaling Axis.Trends in endocrinology and metabolism: TEM · 2018
    Review
  15. Article
  16. Article
  17. 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

13 authors at 5 institutions in 1 country.

Luís BeloDepartamento de Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal; Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, Portugal.
Henrique NascimentoDepartamento de Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal; Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, Portugal.
Michaela KohlovaInstitute for Biomedical Imaging and Life Science (IBILI), Faculdade de Medicina, Universidade de Coimbra, Coimbra, Portugal.
Elsa Bronze-da-RochaDepartamento de Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal; Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, Portugal.
João FernandesDepartamento de Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal; Institute for Biomedical Imaging and Life Science (IBILI), Faculdade de Medicina, Universidade de Coimbra, Coimbra, Portugal.
Elísio CostaDepartamento de Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal; Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, Portugal.
Cristina CatarinoDepartamento de Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal; Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, Portugal.
Luísa AiresCentro de Investigação em Actividade Física, Saúde e Lazer (CIAFEL), Faculdade de Desporto, Universidade do Porto, Porto, Portugal; Instituto Universitário da Maia (ISMAI), Maia, Portugal.
Helena Ferreira MansilhaDepartamento da Infância e Adolescência/Serviço de Pediatria do Centro Hospitalar do Porto, Porto, Portugal.
Petronila Rocha-PereiraCentro de Investigação em Ciências da Saúde, Universidade da Beira Interior, Covilhã, Portugal.
Alexandre QuintanilhaInstituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, Portugal; Instituto de Ciências Biomédicas Abel Salazar (ICBAS), Universidade do Porto, Porto, Portugal.
Carla RêgoCentro da Criança e do Adolescente. Hospital CUF Porto, Center for Health Technology and Services Research (CINTESIS), Faculdade de Medicina, Universidade do Porto, Porto, Portugal.
Alice Santos-SilvaDepartamento de Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal; Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, Portugal.
Universidade do Porto · PTCentro Hospitalar do Porto · PTInstituto Superior da Maia · PTUniversity of Beira Interior · PTUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesBilirubin has potential antioxidant and anti-inflammatory properties. The UGT1A1*28 polymorphism (TA repeats in the promoter region) is a major determinant of bilirubin levels and recent evidence suggests that raised adiposity may also be a contributing factor. We aimed to study the interaction between UGT1A1 polymorphism, hematological and anthropometric variables with total bilirubin levels in young individuals.

methods350 obese (mean age of 11.6 years; 52% females) and 79 controls (mean age of 10.5 years; 59% females) were included. Total bilirubin and C-reactive protein (CRP) plasma levels, hemogram, anthropometric data and UGT1A1 polymorphism were determined. In a subgroup of 74 obese and 40 controls body composition was analyzed by dual-energy X-ray absorptiometry.

resultsThe UGT1A1 genotype frequencies were 49.9%, 42.7% and 7.5% for 6/6, 6/7 and 7/7 genotypes, respectively. Patients with 7/7 genotype presented the highest total bilirubin levels, followed by 6/7 and 6/6 genotypes. Compared to controls, obese patients presented higher erythrocyte count, hematocrit, hemoglobin and CRP levels, but no differences in bilirubin or in UGT1A1 genotype distribution. Body fat percentage was inversely correlated with bilirubin in obese patients but not in controls. This inverse association was observed either in 6/7 or 6/6 genotype obese patients. UGT1A1 polymorphism and body fat percentage were the main factors affecting bilirubin levels within obese patients (linear regression analysis).

conclusionIn obese children and adolescents, body fat composition and UGT1A1 polymorphism are independent determinants of total bilirubin levels. Obese individuals with 6/6 UGT1A1 genotype and higher body fat mass may benefit from a closer clinical follow-up.

Indexed as

Polymorphism, GeneticAdiposityAdolescentAllelesBilirubinCase-Control StudiesChildChild, PreschoolC-Reactive ProteinFemaleGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseGenotypeGlucuronosyltransferaseHumansBilirubinC-Reactive ProteinGlucuronosyltransferaseUGT1A1 Enzyme

Identifiers

PMID24901842
PMCPMC4046990
OpenAlexW2013250018

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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.