Evidence map›Paper›PMID 16725041›Full record

SynthesisBMC medical genetics2006

Meta-analysis on the effect of the N363S polymorphism of the glucocorticoid receptor gene (GRL) on human obesity.

Amelia Marti, M Carmen Ochoa, Almudena Sánchez-Villegas, J Alfredo Martínez, Miguel Angel Martínez-González, Johannes Hebebrand, Anke Hinney, Helmut Vedder

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in BMC medical genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Variation in glucocorticoid sensitivity and the relation with obesity.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Glucocorticoid sensitivity in health and disease.Nature reviews. Endocrinology · 2013
    Review
  11. Article
  12. Article
  13. Recent progress in the genetics of common obesity.British journal of clinical pharmacology · 2009
    Review
  14. Review
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

8 authors at 4 institutions in 2 countries.

Amelia MartiDepartment of Physiology and Nutrition, University of Navarra, Pamplona, Spain. amarti@unav.es
M Carmen Ochoa
Almudena Sánchez-Villegas
J Alfredo Martínez
Miguel Angel Martínez-González
Johannes Hebebrand
Anke Hinney
Helmut Vedder
Universidad de Navarra · ESKliniken Essen-Mitte · DEPhilipps University of Marburg · DEUniversidad de Las Palmas de Gran Canaria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSince both excess glucocorticoid secretion and central obesity are clinical features of some obese patients, it is worthwhile to study a possible association of glucocorticoid receptor gene (GRL) variants with obesity. Previous studies have linked the N363S variant of the GRL gene to increased glucocorticoid effects such as higher body fat, a lower lean-body mass and a larger insulin response to dexamethasone. However, contradictory findings have been also reported about the association between this variant and obesity phenotypes. Individual studies may lack statistical power which may result in disparate results. This limitation can be overcome using meta-analytic techniques.

methodsWe conducted a meta-analysis to assess the association between the N363S polymorphism of the GRL gene and obesity risk. In addition to published research, we included also our own unpublished data -three novel case-control studies- in the meta-analysis The new case-control studies were conducted in German and Spanish children, adolescents and adults (total number of subjects: 1,117). Genotype was assessed by PCR-RFLP (Tsp509I). The final formal meta-analysis included a total number of 5,909 individuals.

resultsThe meta-analysis revealed a higher body mass index (BMI) with an overall estimation of +0.18 kg/m2 (95% CI: +0.004 to +0.35) for homo-/heterozygous carriers of the 363S allele of the GRL gene in comparison to non-carriers. Moreover, differences in pooled BMI were statistically significant and positive when considering one-group studies from the literature in which participants had a BMI below 27 kg/m2 (+ 0.41 kg/m2 [95% CI +0.17 to +0.66]), but the differences in BMI were negative when only our novel data from younger (aged under 45) and normal weight subjects were pooled together (-0.50 kg/m2 [95% CI -0.84 to -0.17]). The overall risk for obesity for homo-/heterozygous carriers of the 363S allele was not statistically significant in the meta-analysis (pooled OR = 1.02; 95% CI: 0.56-1.87).

conclusionAlthough certain genotypic effects could be population-specific, we conclude that there is no compelling evidence that the N363S polymorphism of the GRL gene is associated with either average BMI or obesity risk.

Indexed as

Polymorphism, Single NucleotideAdolescentAdultAmino Acid SubstitutionBody Mass IndexCase-Control StudiesChildFemaleGenetic Predisposition to DiseaseGermanyHumansMaleObesityPhenotypeReceptors, GlucocorticoidSpainReceptors, Glucocorticoid

Identifiers

PMID16725041
PMCPMC1481544
OpenAlexW2130746822

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.