ArticleEndocrinology2010
Developmental programming: differential effects of prenatal testosterone excess on insulin target tissues.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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
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Who cites it
29 citing papers in PubMed, 54 citations in OpenAlex.
- Maternal androgen excess increases the risk of metabolic syndrome in female offspring in their later life: A long-term population-based follow-up study.Archives of gynecology and obstetrics · 2023Article
- The Role of Peroxisome Proliferator-Activated Receptors in Polycystic Ovary Syndrome.Journal of clinical medicine · 2023Review
- Developmental programming: Adipose depot-specific regulation of non-coding RNAs and their relation to coding RNA expression in prenatal testosterone and prenatal bisphenol-A -treated female sheep.Molecular and cellular endocrinology · 2023Article
- Genome-wide DNA methylation pattern in systemic sclerosis microvascular endothelial cells: Identification of epigenetically affected key genes and pathways.Journal of scleroderma and related disorders · 2022Article
- Developmental Programming: Prenatal Testosterone Excess on Liver and Muscle Coding and Noncoding RNA in Female Sheep.Endocrinology · 2022Article
- Developmental programming: Metabolic tissue-specific changes in endoplasmic reticulum stress, mitochondrial oxidative and telomere length status induced by prenatal testosterone excess in the female sheep.Molecular and cellular endocrinology · 2021Article
- Developmental programming: Prenatal testosterone-induced changes in epigenetic modulators and gene expression in metabolic tissues of female sheep.Molecular and cellular endocrinology · 2020Article
- Developmental programming of insulin resistance: are androgens the culprits?The Journal of endocrinology · 2020Review
- Developmental programming: Adipose depot-specific changes and thermogenic adipocyte distribution in the female sheep.Molecular and cellular endocrinology · 2020Article
- Prenatal programming by testosterone of follicular theca cell functions in ovary.Cellular and molecular life sciences : CMLS · 2020Article
- Prenatal Steroids and Metabolic Dysfunction: Lessons from Sheep.Annual review of animal biosciences · 2019Review
- Sex Differences in the Prenatal Programming of Adult Metabolic Syndrome by Maternal Androgens.The Journal of clinical endocrinology and metabolism · 2018Article
- Insulin signaling displayed a differential tissue-specific response to low-dose dihydrotestosterone in female mice.American journal of physiology. Endocrinology and metabolism · 2018Article
- Developmental Programming: Impact of Gestational Steroid and Metabolic Milieus on Mediators of Insulin Sensitivity in Prenatal Testosterone-Treated Female Sheep.Endocrinology · 2017Article
- 11-Oxygenated C19 Steroids Are the Predominant Androgens in Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2017Article
- Gestational Hyperandrogenism in Developmental Programming.Endocrinology · 2017Review
- The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited.Endocrine reviews · 2016 · on this mapReview
- Prenatal programming: adverse cardiac programming by gestational testosterone excess.Scientific reports · 2016Article
- Developmental Programming: Prenatal Testosterone Excess and Insulin Signaling Disruptions in Female Sheep.Biology of reproduction · 2016Article
- Developmental Programming: Impact of Gestational Steroid and Metabolic Milieus on Adiposity and Insulin Sensitivity in Prenatal Testosterone-Treated Female Sheep.Endocrinology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Polycystic ovarian syndrome (PCOS) is the leading cause of infertility in reproductive-aged women with the majority manifesting insulin resistance. To delineate the causes of insulin resistance in women with PCOS, we determined changes in the mRNA expression of insulin receptor (IR) isoforms and members of its signaling pathway in tissues of adult control (n = 7) and prenatal testosterone (T)-treated (n = 6) sheep (100 mg/kg twice a week from d 30-90 of gestation), the reproductive/metabolic characteristics of which are similar to women with PCOS. Findings revealed that prenatal T excess reduced (P < 0.05) expression of IR-B isoform (only isoform detected), insulin receptor substrate-2 (IRS-2), protein kinase B (AKt), peroxisome proliferator-activated receptor-γ (PPARγ), hormone-sensitive lipase (HSL), and mammalian target of rapamycin (mTOR) but increased expression of rapamycin-insensitive companion of mTOR (rictor), and eukaryotic initiation factor 4E (eIF4E) in the liver. Prenatal T excess increased (P < 0.05) the IR-A to IR-B isoform ratio and expression of IRS-1, glycogen synthase kinase-3α and -β (GSK-3α and -β), and rictor while reducing ERK1 in muscle. In the adipose tissue, prenatal T excess increased the expression of IRS-2, phosphatidylinositol 3-kinase (PI3K), PPARγ, and mTOR mRNAs. These findings provide evidence that prenatal T excess modulates in a tissue-specific manner the expression levels of several genes involved in mediating insulin action. These changes are consistent with the hypothesis that prenatal T excess disrupts the insulin sensitivity of peripheral tissues, with liver and muscle being insulin resistant and adipose tissue insulin sensitive.
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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.