Evidence map›Paper›PMID 36339410›Full record

ArticleFrontiers in endocrinology2022

Association of

Joanna Michałowska, Ewa Miller-Kasprzak, Agnieszka Seraszek-Jaros, Adrianna Mostowska, Paweł Bogdański

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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  8. The hidden impact of GLP-1 receptor agonists on endometrial receptivity and implantation.Acta obstetricia et gynecologica Scandinavica · 2025 · on this map
    Review
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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

5 authors at 1 institution in 1 country.

Joanna MichałowskaDepartment of Treatment of Obesity, Metabolic Disorders and Clinical Dietetics, Poznan University of Medical Sciences, Poznan, Poland.
Ewa Miller-KasprzakDepartment of Treatment of Obesity, Metabolic Disorders and Clinical Dietetics, Poznan University of Medical Sciences, Poznan, Poland.
Agnieszka Seraszek-JarosDepartment of Bioinformatics and Computational Biology, Poznan University of Medical Sciences, Poznan, Poland.
Adrianna MostowskaDepartment of Biochemistry and Molecular Biology, Poznan University of Medical Sciences, Poznan, Poland.
Paweł BogdańskiDepartment of Treatment of Obesity, Metabolic Disorders and Clinical Dietetics, Poznan University of Medical Sciences, Poznan, Poland.
Poznan University of Medical Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Obesity is a complex disease associated with excessive fat accumulation and numerous metabolic complications. So far, many factors leading to the development of this disorder have been identified, including genetic susceptibility. Various studies linked Objective: The aim of this study is to investigate the association of two single nucleotide variants of Methods: Normal-weight subjects (n= 340, control group) and subjects with excessive body mass (n = 600, study group) participated in this study. For all participants, anthropometric measurements and metabolic parameters were collected, and genotyping of the two single nucleotide variants of Results: Significant differences in the genotype distribution of rs2268641 were found, where homozygous TT genotype was significantly less frequent in the study group with excessive body mass (OR=0.66; p=0.0298). For rs6923761, A allele and homozygous AA genotype were significantly more frequent in the study group with excessive weight than in the control group (OR=1.27; p=0.0239 and OR=1.69; p=0.0205, respectively). The association of studied variants with metabolic parameters was found for rs6923761. For this variant, AA carriers had higher body mass in comparison to GG carriers (p=0.0246), and AA carriers had higher glucose concentration in comparison to AG carriers (p=0.0498). We did not find an association of rs2268641 and rs6923761 with metabolic syndrome. Conclusion: In our study, AA carriers of rs6923761 had higher risk of excessive body mass, whereas TT carriers of rs2268641 had lower risk of being overweight. Moreover, homozygous carriers of the minor allele of rs6923761 had higher glucose concentration in comparison to heterozygous subjects. None of the studied variants were associated with metabolic syndrome in the studied population.

Indexed as

Glucagon-Like Peptide-1 ReceptorMetabolic SyndromeGlucoseHumansNucleotidesObesityPolandGlucagon-Like Peptide-1 ReceptorGlucoseNucleotidesGLP-1GLP1R genemetabolic healthmetabolic syndromeobesitysingle nucleotide variant

Identifiers

PMID36339410
PMCPMC9626533
OpenAlexW4306849685

What OpenQuestion holds

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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.