Evidence map›Paper›PMID 17694296›Full record

ArticleDiabetologia2007

Anthropometry, carbohydrate and lipid metabolism in the East Flanders Prospective Twin Survey: heritabilities.

N Y Souren, A D C Paulussen, R J F Loos, M Gielen, G Beunen, R Fagard, C Derom, R Vlietinck, M P Zeegers

Open access · hybridAbstract readTwin Study
In one paragraph

Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
14.6field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Variation in the heritability of body mass index based on diverse twin studies: a systematic review.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2013
    Pooled it
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  13. Genomics of body fat distribution.Journal of genetics · 2021
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  19. Insulin Resistance in Children.Frontiers in endocrinology · 2019
    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

9 authors at 4 institutions in 3 countries.

N Y SourenDepartment of Genetics and Cell Biology, Maastricht University, Maastricht, the Netherlands.
A D C Paulussen
R J F Loos
M Gielen
G Beunen
R Fagard
C Derom
R Vlietinck
M P Zeegers
KU Leuven · BEMaastricht University · NLMaastricht University Medical Centre · NLUniversity of Birmingham · GB

Funding

Medical Research Council MC_U106188470
6 · The paper itself

Abstract

aims/hypothesisWe determined the genetic contribution of 18 anthropometric and metabolic risk factors of type 2 diabetes using a young healthy twin population.

methodsTraits were measured in 240 monozygotic (MZ) and 138 dizygotic (DZ) twin pairs aged 18 to 34 years. Twins were recruited from the Belgian population-based East Flanders Prospective Twin Survey, which is characterised by its accurate zygosity determination and extensive collection of perinatal and placental data, including information on chorionicity. Heritability was estimated using structural equation modelling implemented in the Mx software package.

resultsIntra-pair correlations of the anthropometric and metabolic characteristics did not differ between MZ monochorionic and MZ dichorionic pairs; consequently heritabilities were estimated using the classical twin approach. For body mass, BMI and fat mass, quantitative sex differences were observed; genetic variance explained 84, 85 and 81% of the total variation in men and 74, 75 and 70% in women, respectively. Heritability estimates of the waist-to-hip ratio, sum of four skinfold thicknesses and lean body mass were 70, 74 and 81%, respectively. The heritability estimates of fasting glucose, fasting insulin, homeostasis model assessment of insulin resistance and beta cell function, as well as insulin-like growth factor binding protein-1 levels were 67, 49, 48, 62 and 47%, in that order. Finally, for total cholesterol, LDL-cholesterol, HDL-cholesterol, total cholesterol:HDL-cholesterol ratio, triacylglycerol, NEFA and leptin levels, genetic factors explained 75, 78, 76, 79, 58, 37 and 53% of the total variation, respectively. CONCLUSIONS/

interpretationGenetic factors explain the greater part of the variation in traits related to obesity, glucose intolerance/insulin resistance and dyslipidaemia.

Indexed as

AnthropometryBody Mass IndexAdipose TissueAdolescentAdultAnalysis of VarianceBelgiumBody SizeDietary CarbohydratesDietary FatsFemaleGenetic VariationHumansLipidsMaleSkinfold ThicknessDietary CarbohydratesDietary FatsLipidsTriglycerides

Identifiers

PMID17694296
PMCPMC2039867
OpenAlexW2026446409

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.