Evidence map›Paper›PMID 25942654›Full record

ReviewNature reviews. Endocrinology2015

Genetics of androgen metabolism in women with infertility and hypoandrogenism.

Aya Shohat-Tal, Aritro Sen, David H Barad, Vitaly Kushnir, Norbert Gleicher

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  16. More on the conversion of DHEA to testosterone.Nature reviews. Endocrinology · 2015
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Aya Shohat-TalCenter for Human Reproduction, 21 E. 69th Street, New York, NY 10021, USA.
Aritro SenDepartment of Internal Medicine, Division of Endocrinology and Metabolism, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA.
David H BaradCenter for Human Reproduction, 21 E. 69th Street, New York, NY 10021, USA.
Vitaly KushnirCenter for Human Reproduction, 21 E. 69th Street, New York, NY 10021, USA.
Norbert GleicherCenter for Human Reproduction, 21 E. 69th Street, New York, NY 10021, USA.
Center for Human Reproduction · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoandrogenism in women with low functional ovarian reserve (LFOR, defined as an abnormally low number of small growing follicles) adversely affects fertility. The androgen precursor dehydroepiandrosterone (DHEA) is increasingly used to supplement treatment protocols in women with LFOR undergoing in vitro fertilization. Due to differences in androgen metabolism, however, responses to DHEA supplementation vary between patients. In addition to overall declines in steroidogenic capacity with advancing age, genetic factors, which result in altered expression or enzymatic function of key steroidogenic proteins or their upstream regulators, might further exacerbate variations in the conversion of DHEA to testosterone. In this Review, we discuss in vitro studies and animal models of polymorphisms and gene mutations that affect the conversion of DHEA to testosterone and attempt to elucidate how these variations affect female hormone profiles. We also discuss treatment options that modulate levels of testosterone by targeting the expression of steroidogenic genes. Common variants in genes encoding DHEA sulphotransferase, aromatase, steroid 5α-reductase, androgen receptor, sex-hormone binding globulin, fragile X mental retardation protein and breast cancer type 1 susceptibility protein have been implicated in androgen metabolism and, therefore, can affect levels of androgens in women. Short of screening for all potential genetic variants, hormonal assessments of patients with low testosterone levels after DHEA supplementation facilitate identification of underlying genetic defects. The genetic predisposition of patients can then be used to design individualized fertility treatments.

Indexed as

3-Oxo-5-alpha-Steroid 4-DehydrogenaseAndrogensAnimalsAromataseDehydroepiandrosteroneDisease Models, AnimalFemaleFragile X Messenger Ribonucleoprotein 1Genes, BRCA1HumansInfertility, FemaleOvarian ReservePolymorphism, GeneticReceptors, AndrogenSex Hormone-Binding GlobulinSulfotransferases3-Oxo-5-alpha-Steroid 4-DehydrogenaseAndrogensAromataseDehydroepiandrosteronedehydroepiandrosterone sulfotransferaseFragile X Messenger Ribonucleoprotein 1Receptors, AndrogenSex Hormone-Binding GlobulinSulfotransferasesTestosterone

Identifiers

PMID25942654
OpenAlexW1565593844

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.