Evidence map›Paper›PMID 18757445›Full record

ArticleHuman reproduction (Oxford, England)2008

FEM1A and FEM1B: novel candidate genes for polycystic ovary syndrome.

M O Goodarzi, J F Maher, J Cui, X Guo, K D Taylor, R Azziz

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Human reproduction (Oxford, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.8field-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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. International journal of molecular sciences · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Fem1b promotes ubiquitylation and suppresses transcriptional activity of Gli1.Biochemical and biophysical research communications · 2013
    Article
  10. Article
  11. Family-based analysis of candidate genes for polycystic ovary syndrome.The Journal of clinical endocrinology and metabolism · 2010
    Article
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

6 authors at 3 institutions in 1 country.

M O GoodarziDepartment of Medicine, Division of Endocrinology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
J F Maher
J Cui
X Guo
K D Taylor
R Azziz
Cedars-Sinai Medical Center · USThe University of Texas Southwestern Medical Center · USUniversity of California, Los Angeles · US

Funding

ZONA-FREE HAMSTER OVA ASSAY AS AN INDICATOR OF MALE FERTILITYM01RR000425 · NCRR · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI ANDERSON, GAIL V · 1985 to 2011
$74.2M
ADRENAL ANDROGEN EXCESS IN THE POLYCYSTIC OVARY SYNDROMER01HD029364 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AZZIZ, RICARDO · 1993 to 2011
$2.2M
ANDROGEN EXCESS DISORDERK24HD001346 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AZZIZ, RICARDO · 2000 to 2004
$455k
NCRR NIH HHS M01 RR000425NCRR NIH HHS M01-RR00425NICHD NIH HHS K24 HD001346NICHD NIH HHS K24-HD01346NICHD NIH HHS R01 HD029364NICHD NIH HHS R01-HD29364
6 · The paper itself

Abstract

backgroundHuman homologs (FEM1A, FEM1B, FEM1C) of nematode sex determination genes are candidate genes for polycystic ovary syndrome (PCOS). We previously identified a FEM1A mutation (H500Y) in a woman with PCOS; FEM1B has been implicated in insulin secretion.

methodsWomen with and without PCOS (287 cases, 187 controls) were genotyped for H500Y and six FEM1A single nucleotide polymorphisms (SNPs), five FEM1B SNPs and five FEM1C SNPs. SNPs and haplotypes were determined and tested for association with PCOS and component phenotypes.

resultsNo subject carried the FEM1A H500Y mutation. FEM1A SNPs rs8111933 (P = 0.001) and rs12460989 (P = 0.046) were associated with an increased likelihood of PCOS whereas FEM1A SNP rs1044386 was associated with a reduced probability of PCOS (P = 0.013). FEM1B SNP rs10152450 and a linked SNP were associated with a reduced likelihood of PCOS (P = 0.005), and lower homeostasis model assessment (HOMA) for beta-cell function (HOMA-%B, P = 0.011) and lower HOMA for insulin resistance (HOMA-IR, P = 0.018). FEM1B SNP rs12909277 was associated with lower HOMA-%B (P = 0.008) and lower HOMA-IR (P = 0.037). Haplotype associations were consistent with SNP results, and also revealed association of FEM1B haplotype TGAGG with increased HOMA-%B (P = 0.007) and HOMA-IR (P = 0.024). FEM1C variants were not associated with PCOS.

conclusionsThis study presents evidence suggesting a role for FEM1A and FEM1B in the pathogenesis of PCOS. Only FEM1B variants were associated with insulin-related traits in PCOS women, consistent with prior evidence linking this gene to insulin secretion. Replication of these associations and mechanistic studies will be necessary to establish the role of these genes in PCOS.

Indexed as

AdolescentAdultCarrier ProteinsCell Cycle ProteinsFemaleGene FrequencyHaplotypesHumansInsulinInsulin ResistanceInsulin SecretionMiddle AgedPolycystic Ovary SyndromePolymorphism, Single NucleotideProteinsRisk FactorsCarrier ProteinsCell Cycle ProteinsFEM1A protein, humanFEM1B protein, humanFEM1C protein, humanInsulinProteinsUbiquitin-Protein Ligase Complexes

Identifiers

PMID18757445
PMCPMC2583941
OpenAlexW2145248749

What OpenQuestion holds

Textmetadata
LicenceTDM
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.