Evidence map›Paper›PMID 32325455›Full record

ArticleObesity facts2020

Genetic Variants in the Activation of the Brown-Like Adipocyte Pathway and the Risk for Severe Obesity.

Ana Carolina Proença da Fonseca, Guilherme Proença da Fonseca, Bruna Marchesini, Danielle Dutra Voigt, Mario Campos Junior, Verônica Marques Zembrzuski, João Regis Ivar Carneiro, José Firmino Nogueira Neto, Pedro Hernan Cabello, Giselda Maria Kalil Cabello

Open access · goldAbstract read
In one paragraph

Article in Obesity facts, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    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

10 authors at 4 institutions in 1 country.

Ana Carolina Proença da FonsecaHuman Genetics Laboratory, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro, Brazil, ana_carol_pf@hotmail.com.
Guilherme Proença da FonsecaHuman Genetics Laboratory, Grande Rio University, Rio de Janeiro, Brazil.
Bruna MarchesiniHuman Genetics Laboratory, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro, Brazil.
Danielle Dutra VoigtHuman Genetics Laboratory, Grande Rio University, Rio de Janeiro, Brazil.
Mario Campos JuniorHuman Genetics Laboratory, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro, Brazil.
Verônica Marques ZembrzuskiHuman Genetics Laboratory, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro, Brazil.
João Regis Ivar CarneiroClementino Fraga Filho University Hospital, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
José Firmino Nogueira NetoDepartment of Pathology and Laboratory<italic>,</italic>Rio de Janeiro State University, Rio de Janeiro, Brazil.
Pedro Hernan CabelloHuman Genetics Laboratory, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro, Brazil.
Giselda Maria Kalil CabelloHuman Genetics Laboratory, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro, Brazil.
Fundação Oswaldo Cruz · BRUniversidade Unigranrio · BRUniversidade do Estado do Rio de Janeiro · BRUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRegular physical activity has an important role in energy expenditure and combats the development of obesity. During exercise, PPARGC1A is overexpressed, stimulating an increase of the expression of FNDC5. This protein is cleaved to release the hormone irisin, which activates a browning process in white adipose tissue through an increase in UCP1 expression. As a result, irisin leads to mitochondrial heat production and energy expenditure.

objectivesThe aim of this study was to investigate whether genetic variants in genes related to browning are associated with severe obesity and obesity-related features. This case-control study comprised 210 individuals with severe obesity (median body mass index [BMI] 45.6 [range 40.5-52.2]) and 191 normal-weight subjects (BMI 22.8 [21.1-23.9]).

methodsGenomic DNA was extracted from peripheral blood and the genotypes of the PPARGC1A(rs8192678, rs3736265, rs2970847, and rs3755863) and UCP1 (rs6536991 and rs12502572) genes were obtained using Taqman® assay. For the FNDC5 gene, screening of exons 3-5 as well as their intron-exon boundaries was performed using automatic sequencing.

resultsOur results demonstrated that PPARGC1Ars2970847 and UCP1rs12502572 are associated with severe obesity. Furthermore, these polymorphisms influence anthropometric traits, such as BMI, body weight, and body adiposity index. Our findings also showed a dose-effect relationship between PPARGC1A rs8192678 and fasting plasma glucose. Finally, 5 rare mutations were identified in FNDC5, and 1 of these is a novel missense mutation.

conclusionThis study shows that genetic variants in the activation of brown-like adipocyte pathway play an important role in the susceptibility to severe obesity.

Indexed as

Polymorphism, Single NucleotideAdipocytesAdipocytes, BrownAdipose Tissue, BrownAdipose Tissue, WhiteAdolescentAdultAgedBody Mass IndexCase-Control StudiesCell TransdifferentiationCross-Sectional StudiesEnergy MetabolismFemaleFibronectinsGenotypeFibronectinsFNDC5 protein, humanPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanIrisinPolymorphismPPARGC1ASevere obesityUCP1

Identifiers

PMID32325455
PMCPMC7250364
OpenAlexW3017412456

What OpenQuestion holds

Textmetadata
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.