Evidence map›Paper›PMID 27538985›Full record

ArticleBMC genetics2016

Associations of genetic risk scores based on adult adiposity pathways with childhood growth and adiposity measures.

Claire Monnereau, Suzanne Vogelezang, Claudia J Kruithof, Vincent W V Jaddoe, Janine F Felix

Open access · diamondAbstract read
In one paragraph

Article in BMC genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 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

5 authors at 1 institution in 1 country.

Claire MonnereauThe Generation R Study Group, Erasmus MC, University Medical Center Rotterdam, P.O. Box 2040, 3000, CA, Rotterdam, The Netherlands.
Suzanne VogelezangThe Generation R Study Group, Erasmus MC, University Medical Center Rotterdam, P.O. Box 2040, 3000, CA, Rotterdam, The Netherlands.
Claudia J KruithofThe Generation R Study Group, Erasmus MC, University Medical Center Rotterdam, P.O. Box 2040, 3000, CA, Rotterdam, The Netherlands.
Vincent W V JaddoeThe Generation R Study Group, Erasmus MC, University Medical Center Rotterdam, P.O. Box 2040, 3000, CA, Rotterdam, The Netherlands.
Janine F FelixThe Generation R Study Group, Erasmus MC, University Medical Center Rotterdam, P.O. Box 2040, 3000, CA, Rotterdam, The Netherlands. j.felix@erasmusmc.nl.
Erasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundResults from genome-wide association studies (GWAS) identified many loci and biological pathways that influence adult body mass index (BMI). We aimed to identify if biological pathways related to adult BMI also affect infant growth and childhood adiposity measures.

methodsWe used data from a population-based prospective cohort study among 3,975 children with a mean age of 6 years. Genetic risk scores were constructed based on the 97 SNPs associated with adult BMI previously identified with GWAS and on 28 BMI related biological pathways based on subsets of these 97 SNPs. Outcomes were infant peak weight velocity, BMI at adiposity peak and age at adiposity peak, and childhood BMI, total fat mass percentage, android/gynoid fat ratio, and preperitoneal fat area. Analyses were performed using linear regression models.

resultsA higher overall adult BMI risk score was associated with infant BMI at adiposity peak and childhood BMI, total fat mass, android/gynoid fat ratio, and preperitoneal fat area (all p-values < 0.05). Analyses focused on specific biological pathways showed that the membrane proteins genetic risk score was associated with infant peak weight velocity, and the genetic risk scores related to neuronal developmental processes, hypothalamic processes, cyclicAMP, WNT-signaling, membrane proteins, monogenic obesity and/or energy homeostasis, glucose homeostasis, cell cycle, and muscle biology pathways were associated with childhood adiposity measures (all p-values <0.05). None of the pathways were associated with childhood preperitoneal fat area.

conclusionsA genetic risk score based on 97 SNPs related to adult BMI was associated with peak weight velocity during infancy and general and abdominal fat measurements at the age of 6 years. Risk scores based on genetic variants linked to specific biological pathways, including central nervous system and hypothalamic processes, influence body fat development from early life onwards.

Indexed as

AdiposityChild DevelopmentMetabolic Networks and PathwaysBody Mass IndexChildFemaleGenetic Predisposition to DiseaseHumansInfantMaleNetherlandsObesityOverweightPolymorphism, Single NucleotideBody mass indexGeneticsGenome-wide association studyPediatricsPolymorphism, single nucleotide

Identifiers

PMID27538985
PMCPMC4991119
OpenAlexW2515470493

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.