ArticleBiology of reproduction2016
Developmental Programming: Prenatal Testosterone Excess and Insulin Signaling Disruptions in Female Sheep.
Article in Biology of reproduction, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Serum free and bioavailable rather than total testosterone is associated with the progression of non-alcoholic fatty liver disease in postmenopausal women: a prospective study.Frontiers in endocrinology · 2026Article
- Developmental programming: Differing impact of prenatal testosterone and prenatal bisphenol-A -treatment on hepatic methylome in female sheep.Molecular and cellular endocrinology · 2025Article
- Gender difference in the association between serum uric acid and metabolic dysfunction-associated steatotic liver disease in patients with newly diagnosed type 2 diabetes.BMC gastroenterology · 2025Article
- Developmental programming: Testosterone excess masculinizes female pancreatic transcriptome and function in sheep.Molecular and cellular endocrinology · 2024Article
- Placental mRNA Expression of Neurokinin B Is Increased in PCOS Pregnancies with Female Offspring.Biomedicines · 2024Article
- The Influences of Perinatal Androgenic Exposure on Cardiovascular and Metabolic Disease of Offspring of PCOS.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Western-style diet in the presence of elevated circulating testosterone induces adipocyte hypertrophy without proinflammatory responses in rhesus macaques.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- 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
- Role of Hormones During Gestation and Early Development: Pathways Involved in Developmental Programming.Advances in experimental medicine and biology · 2023Article
- Developmental Programming: Prenatal Testosterone Excess on Liver and Muscle Coding and Noncoding RNA in Female Sheep.Endocrinology · 2022Article
- Developmental programming of offspring adipose tissue biology and obesity risk.International journal of obesity (2005) · 2021Review
- 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: Adipose depot-specific transcriptional regulation by prenatal testosterone excess in a sheep model of PCOS.Molecular and cellular endocrinology · 2021Article
- Developmental programming: Prenatal testosterone excess disrupts pancreatic islet developmental trajectory in female sheep.Molecular and cellular endocrinology · 2020Article
- Developmental programming: gestational testosterone excess disrupts LH secretion in the female sheep fetus.Reproductive biology and endocrinology : RB&E · 2020Article
- Developmental programming: Transcriptional regulation of visceral and subcutaneous adipose by prenatal bisphenol-A in female sheep.Chemosphere · 2020Article
- Developmental programming: Prenatal testosterone-induced changes in epigenetic modulators and gene expression in metabolic tissues of female sheep.Molecular and cellular endocrinology · 2020Article
- Animal Models to Understand the Etiology and Pathophysiology of Polycystic Ovary Syndrome.Endocrine reviews · 2020Review
- 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
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Women with polycystic ovary syndrome often manifest insulin resistance. Using a sheep model of polycystic ovary syndrome-like phenotype, we explored the contribution of androgen and insulin in programming and maintaining disruptions in insulin signaling in metabolic tissues. Phosphorylation of AKT, ERK, GSK3beta, mTOR, and p70S6K was examined in the liver, muscle, and adipose tissue of control and prenatal testosterone (T)-, prenatal T plus androgen antagonist (flutamide)-, and prenatal T plus insulin sensitizer (rosiglitazone)-treated fetuses as well as 2-yr-old females. Insulin-stimulated phospho (p)-AKT was evaluated in control and prenatal T-, prenatal T plus postnatal flutamide-, and prenatal T plus postnatal rosiglitazone-treated females at 3 yr of age. GLUT4 expression was evaluated in the muscle at all time points. Prenatal T treatment increased mTOR, p-p70S6K, and p-GSK3beta levels in the fetal liver with both androgen antagonist and insulin sensitizer preventing the mTOR increase. Both interventions had partial effect in preventing the increase in p-GSK3beta. In the fetal muscle, prenatal T excess decreased p-GSK3beta and GLUT4. The decrease in muscle p-GSK3beta was partially prevented by insulin sensitizer cotreatment. Both interventions partially prevented the decrease in GLUT4. Prenatal T treatment had no effect on basal expression of any of the markers in 2-yr-old females. At 3 yr of age, prenatal T treatment prevented the insulin-stimulated increase in p-AKT in liver and muscle, but not in adipose tissue, and neither postnatal intervention restored p-AKT response to insulin stimulation. Our findings provide evidence that prenatal T excess changes insulin sensitivity in a tissue- and development-specific manner and that both androgens and insulin may be involved in the programming of these metabolic disruptions.
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Registered trials
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