ArticleDiabetes care2008
First evidence of genetic association between AKT2 and polycystic ovary syndrome.
Article in Diabetes care, 2008. 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 11 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Evaluating reported candidate gene associations with polycystic ovary syndrome.Fertility and sterility · 2013Pooled it
- Trial
- In utero exposure to acetaminophen and ibuprofen leads to intergenerational accelerated reproductive aging in female mice.Communications biology · 2019Article
- Effect of maternal PCOS and PCOS-like phenotype on the offspring's health.Molecular and cellular endocrinology · 2016Review
- Sirolimus and Everolimus Pathway: Reviewing Candidate Genes Influencing Their Intracellular Effects.International journal of molecular sciences · 2016Review
- Loss of PKBβ/Akt2 predisposes mice to ovarian cyst formation and increases the severity of polycystic ovary formation in vivo.Disease models & mechanisms · 2012Article
- Article
- Replication of association of a novel insulin receptor gene polymorphism with polycystic ovary syndrome.Fertility and sterility · 2011Article
- Article
- Epigenetics in polycystic ovary syndrome: a pilot study of global DNA methylation.Fertility and sterility · 2010Article
- Molecular crosstalk between insulin-like growth factors and follicle-stimulating hormone in the regulation of granulosa cell function.Reproductive medicine and biologyReview
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveInsulin resistance has been reported in up to 70% of women with polycystic ovary syndrome (PCOS). Physiologic and genetic data currently implicate post-insulin receptor signaling defects in substrates such as glycogen synthase kinase 3beta (GSK3beta). The AKT2 gene was chosen as a candidate for PCOS because its product affects glucose metabolism and mitogenic signaling, interacts with GSK3beta, and mediates cell survival in the ovary. RESEARCH DESIGN AND
methodsSubjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham, and control subjects were recruited from the surrounding community; 287 white women with PCOS and 187 white control subjects were genotyped for four single nucleotide polymorphisms (SNPs) in AKT2. Genotyping took place at Cedars-Sinai Medical Center in Los Angeles. SNPs and haplotypes were tested for association with PCOS risk and phenotypic markers of PCOS.
resultsMinor allele carriers of SNPs rs3730051 and rs8100018 had increased odds of PCOS (odds ratio [OR] 2.2, P = 0.004, and 2.4, P = 0.001, respectively). The haplotype T-G-C-T was significantly associated with PCOS (OR 2.0, P = 0.01). Carriers of the risk haplotypes for both AKT2 and GSK3B had a further increased odds of PCOS (OR 3.1, P = 0.005).
conclusionsThese data suggest that polymorphisms in two components of the insulin signaling pathway, AKT2 and GSK3B, are associated with PCOS. The presence of multiple lesions in a single pathway may confer increased risk.
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Registered trials
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.