Evidence map›Paper›PMID 22801903›Full record

SynthesisDiabetologia2012

Impact of FTO genotypes on BMI and weight in polycystic ovary syndrome: a systematic review and meta-analysis.

P Wojciechowski, A Lipowska, P Rys, K G Ewens, S Franks, S Tan, E Lerchbaum, J Vcelak, R Attaoua, M Straczkowski and 13 more

Erratum issuedOpen access · hybridAbstract readMeta-AnalysisMulticenter StudySystematic Review
In one paragraph

Synthesis in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 7 pooled it
12.7field-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

46 citing papers in PubMed, 7 syntheses or guidelines pooled it, 107 citations in OpenAlex.

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  12. A novel link betweenBiomedical reports · 2025
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

23 authors at 15 institutions in 7 countries.

P WojciechowskiHTA Consulting, Krakow, Poland.
A LipowskaSchool of Medicine, Emory University, Atlanta, GA, USA.
P RysHTA Consulting, Krakow, Poland.
K G EwensDepartment of Genetics, School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
S FranksInstitute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Hospital, London, UK.
S TanDepartment of Endocrinology, University of Duisburg-Essen, Essen, Germany.
E LerchbaumDepartment of Internal Medicine, Division of Endocrinology and Metabolism, Medical University of Graz, Graz, Austria.
J VcelakInstitute of Endocrinology, Prague, Czech Republic.
R AttaouaMolecular Endocrinology Laboratory, UMR-204 NUTRIPASS, Institut Universitaire de Recherche Clinique (IURC), Montpellier, France.
M StraczkowskiDepartment of Endocrinology, Diabetology and Internal Medicine, Medical University of Bialystok, Bialystok, Poland.
R AzzizDepartment of Obstetrics and Gynecology, Georgia Health Sciences University, Augusta, GA, USA.
T M BarberDepartment of Metabolic and Vascular Health, Clinical Sciences Research Laboratories, Warwick Medical School, Coventry, UK.
A HinneyDepartment of Child and Adolescent Psychiatry, University of Duisburg-Essen, Essen, Germany.
B Obermayer-PietschDepartment of Internal Medicine, Division of Endocrinology and Metabolism, Medical University of Graz, Graz, Austria.
P LukasovaInstitute of Endocrinology, Prague, Czech Republic.
B BendlovaInstitute of Endocrinology, Prague, Czech Republic.
F GrigorescuMolecular Endocrinology Laboratory, UMR-204 NUTRIPASS, Institut Universitaire de Recherche Clinique (IURC), Montpellier, France.
I KowalskaDepartment of Endocrinology, Diabetology and Internal Medicine, Medical University of Bialystok, Bialystok, Poland.
M O GoodarziDivision of Endocrinology, Diabetes, and Metabolism, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
GIANT Consortium
J F StraussDepartment of Obstetrics and Gynecology, Virginia Commonwealth University, Richmond, VA, USA.
M I McCarthyWellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
M T MaleckiDepartment of Metabolic Diseases, Jagiellonian University Medical College, 15 Kopernika Street, 31-501, Krakow, Poland. malecki_malecki@yahoo.com.
Institute of Endocrinology · CZCRE Consulting (Poland) · PLInstitut Universitaire de Recherche Clinique · FRMedical University of Białystok · PLMedical University of Graz · ATUniversity of Duisburg-Essen · DEAugusta University Health · USCedars-Sinai Medical Center · USCentre for Human Genetics · GBEmory University · USHammersmith Hospital · GBJagiellonian University · PLUniversity of Pennsylvania · USUniversity of Warwick · GBVirginia Commonwealth University · US

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MILES Frome WILKINSON · 2003 to 2026
$40.4M
Translational Research in Polycystic Ovary SyndromeU54HD034449 · NICHD · VIRGINIA COMMONWEALTH UNIVERSITY · PI NESTLER, JOHN E · 1997 to 2012
$15.0M
Medical Research Council G0802782NICHD NIH HHS U54 HD034449NIDDK NIH HHS P30 DK063491Wellcome Trust 090532
6 · The paper itself

Abstract

aims/hypothesisFTO gene single nucleotide polymorphisms (SNPs) have been shown to be associated with obesity-related traits and type 2 diabetes. Several small studies have suggested a greater than expected effect of the FTO rs9939609 SNP on weight in polycystic ovary syndrome (PCOS). We therefore aimed to examine the impact of FTO genotype on BMI and weight in PCOS.

methodsA systematic search of medical databases (PubMed, EMBASE and Cochrane CENTRAL) was conducted up to the end of April 2011. Seven studies describing eight distinct PCOS cohorts were retrieved; seven were genotyped for SNP rs9939609 and one for SNP rs1421085. The per allele effect on BMI and body weight increase was calculated and subjected to meta-analysis.

resultsA total of 2,548 women with PCOS were included in the study; 762 were TT homozygotes, 1,253 had an AT/CT genotype, and 533 were AA/CC homozygotes. Each additional copy of the effect allele (A/C) increased the BMI by a mean of 0.19 z score units (95% CI 0.13, 0.24; p = 2.26 × 10(-11)) and body weight by a mean of 0.20 z score units (95% CI 0.14, 0.26; p = 1.02 × 10(-10)). This translated into an approximately 3.3 kg/m(2) increase in BMI and an approximately 9.6 kg gain in body weight between TT and AA/CC homozygotes. The association between FTO genotypes and BMI was stronger in the cohorts with PCOS than in the general female populations from large genome-wide association studies. Deviation from an additive genetic model was observed in heavier populations. CONCLUSIONS/

interpretationThe effect of FTO SNPs on obesity-related traits in PCOS seems to be more than two times greater than the effect found in large population-based studies. This suggests an interaction between FTO and the metabolic context or polygenic background of PCOS.

Indexed as

Body Mass IndexGenotypeAdultAlpha-Ketoglutarate-Dependent Dioxygenase FTOBody WeightFemaleHumansObesityOutcome Assessment, Health CarePolycystic Ovary SyndromePolymorphism, Single NucleotideProteinsAlpha-Ketoglutarate-Dependent Dioxygenase FTOFTO protein, humanProteins

Identifiers

PMID22801903
PMCPMC3433670
OpenAlexW2056017663

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.