Evidence map›Paper›PMID 36810017›Full record

ArticleBMC pediatrics2023

The influence of six polymorphisms of uncoupling protein 3 (UCP3) gene and childhood obesity: a case-control study.

Jakeline S Fortes, Renata M Pinto, Raissa F de Souza, Fernanda R Godoy, Raphael S da Cruz, Daniela de M E Silva, Hugo P Leite Filho, Aparecido D da Cruz, Lysa B Minasi

Open access · goldAbstract read
In one paragraph

Article in BMC pediatrics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 51% 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 citations in OpenAlex.

  1. Article
  2. Synthetic Polymers for Drug, Gene, and Vaccine Delivery.Polymer science & technology (Washington, D.C.) · 2025
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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

9 authors at 4 institutions in 1 country.

Jakeline S FortesReplicon Research Group, Genetics Graduate Program, School of Medical and Life Sciences, Pontifical Catholic University of Goiás, Rua 235, N. 40, Setor Leste Universitário, Goiânia, GO, 74605-050, Brazil.
Renata M PintoPediatrics Department, Federal University of Goiás, Câmpus Colemar Natal E Silva (Câmpus I), Rua 235, Setor Leste Universitário, Goiânia, GO, Brazil.
Raissa F de SouzaReplicon Research Group, Genetics Graduate Program, School of Medical and Life Sciences, Pontifical Catholic University of Goiás, Rua 235, N. 40, Setor Leste Universitário, Goiânia, GO, 74605-050, Brazil.
Fernanda R GodoyReplicon Research Group, Genetics Graduate Program, School of Medical and Life Sciences, Pontifical Catholic University of Goiás, Rua 235, N. 40, Setor Leste Universitário, Goiânia, GO, 74605-050, Brazil.
Raphael S da CruzReplicon Research Group, Genetics Graduate Program, School of Medical and Life Sciences, Pontifical Catholic University of Goiás, Rua 235, N. 40, Setor Leste Universitário, Goiânia, GO, 74605-050, Brazil.
Daniela de M E SilvaGenetics and Molecular Biology Graduate Program, Federal University of Goiás, Campus Samambaia, Goiânia, GO, 74690-900, Brazil.
Hugo P Leite FilhoGoiás State University, Ceres Campus, Ceres, GO, Brazil.
Aparecido D da CruzReplicon Research Group, Genetics Graduate Program, School of Medical and Life Sciences, Pontifical Catholic University of Goiás, Rua 235, N. 40, Setor Leste Universitário, Goiânia, GO, 74605-050, Brazil.
Lysa B MinasiReplicon Research Group, Genetics Graduate Program, School of Medical and Life Sciences, Pontifical Catholic University of Goiás, Rua 235, N. 40, Setor Leste Universitário, Goiânia, GO, 74605-050, Brazil. minasi@pucgoias.edu.br.
Pontifícia Universidade Católica de Goiás · BRUniversidade Federal de Goiás · BRFundação de Apoio a Pesquisa do Estado de Goiás · BRUniversidade Estadual de Goiás · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity is defined as a multifactorial disease, marked by excessive accumulation of body fat, responsible for compromising the individual's health over the years. The energy balance is essential for the proper functioning of the body, as the individual needs to earn and spend energy in a compensatory way. Mitochondrial Uncoupling Proteins (UCP) help in energy expenditure through heat release and genetic polymorphisms could be responsible for reducing energy consumption to release heat and consequently generate an excessive accumulation of fat in the body. Thus, this study aimed to investigate the potential association between six UCP3 polymorphisms, that have not yet been represented in ClinVar®, and pediatric obesity susceptibility.

methodsA case-control study was conducted with 225 children from Central Brazil. The groups were subdivided into obese (123) and eutrophic (102) individuals. The polymorphisms rs15763, rs1685354, rs1800849, rs11235972, rs647126, and rs3781907 were determined by real-time Polymerase Chain Reaction (qPCR).

resultsBiochemical and anthropometric evaluation of obese group showed higher levels of triglycerides, insulin resistance, and LDL-C and low level of HDL-C. Insulin resistance, age, sex, HDL-C, fasting glucose, triglyceride levels, and parents' BMI explained up to 50% of body mass deposition in the studied population. Additionally, obese mothers contribute 2 × more to the Z-BMI of their children than the fathers. The SNP rs647126 contributed to 20% to the risk of obesity in children and the SNP rs3781907 contribute to 10%. Mutant alleles of UCP3 increase the risk for triglycerides, total cholesterol, and HDL-C levels. The polymorphism rs3781907 is the only one that could not be a biomarker for obesity as the risk allele seem to be protective gains the increase in Z-BMI in our pediatric population. Haplotype analysis demonstrated two SNP blocks (rs15763, rs647126, and rs1685534) and (rs11235972 and rs1800849) that showed linkage disequilibrium, with LOD 76.3% and D' = 0.96 and LOD 57.4% and D' = 0.97, respectively.

conclusionsThe causality between UCP3 polymorphism and obesity were not detected. On the other hand, the studied polymorphism contributes to Z-BMI, HOMA-IR, triglycerides, total cholesterol, and HDL-C levels. Haplotypes are concordant with the obese phenotype and contribute minimally to the risk of obesity.

Indexed as

Insulin ResistancePediatric ObesityUncoupling Protein 3Body Mass IndexCase-Control StudiesChildCholesterolGene FrequencyGenotypeHumansPolymorphism, Single NucleotideTriglyceridesCholesterolTriglyceridesUCP3 protein, humanUncoupling Protein 3HDLInsulin resistanceMitochondrial Uncoupling ProteinZ- BMI

Identifiers

PMID36810017
PMCPMC9942342
OpenAlexW4321457859

What Socratic 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 Socratic graph.