Research Output
In an ovine model of polycystic ovary syndrome (PCOS) prenatal androgens suppress female fetal renal gluconeogenesis.
  Increased maternal androgen exposure during pregnancy programmes a polycystic ovary syndrome (PCOS)-like condition, with metabolic dysfunction, in adult female offspring. Other in utero exposures associated with the development of insulin resistance, such as intrauterine growth restriction and exposure to prenatal glucocorticoids, are associated with altered fetal gluconeogenesis. We therefore aimed to assess the effect of maternal androgenisation on the expression of PEPCK and G6PC in the ovine fetus. Pregnant Scottish Greyface sheep were treated with twice weekly testosterone propionate (TP; 100mg) or vehicle control from day 62 to day102 of gestation. At day 90 and day 112 fetal plasma and liver and kidney tissue was collected for analysis. PEPCK and G6PC expression were analysed by quantitative RT-PCR, immunohistochemistry and western blotting. PEPCK and G6PC were localised to fetal hepatocytes but maternal androgens had no effect on female or male fetuses. PEPCK and G6PC were also localised to the renal tubules and renal PEPCK (P

  • Type:

    Article

  • Date:

    06 July 2015

  • Publication Status:

    Published

  • DOI:

    10.1371/journal.pone.0132113

  • ISSN:

    1932-6203

  • Library of Congress:

    RG Gynecology and obstetrics

  • Dewey Decimal Classification:

    618 Gynecology, obstetrics, pediatrics & geriatrics

  • Projects:

    G0500717; G0901807;

  • Funders:

    Medical Research Council

Citation

Kanellopoulos-Langevin, C., Connolly, F., Rae, M. T., Späth, K., Boswell, L., McNeilly, A. S., & Duncan, W. C. (2015). In an ovine model of polycystic ovary syndrome (PCOS) prenatal androgens suppress female fetal renal gluconeogenesis. PLOS ONE, 10, https://doi.org/10.1371/journal.pone.0132113

Authors

Keywords

Maternal androgen exposure; ovary syndrome (PCOS)-like condition; metabolic dysfunction; in utero exposures;

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