In an ovine model of polycystic ovary syndrome (PCOS) prenatal androgens suppress female fetal renal gluconeogenesis.

Abstract

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

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

• Journal Article Type: Article
• Acceptance Date: Jun 10, 2015
• Online Publication Date: Jul 6, 2015
• Publication Date: Jul 6, 2015
• Deposit Date: Oct 27, 2015
• Publicly Available Date: Aug 26, 2019
• Print ISSN: 1932-6203
• Publisher: Public Library of Science
• Peer Reviewed: Peer Reviewed
• Volume: 10
• Article Number: e0132113
• DOI: https://doi.org/10.1371/journal.pone.0132113
• Keywords: Maternal androgen exposure; ovary syndrome (PCOS)-like condition; metabolic dysfunction; in utero exposures
• Public URL: http://researchrepository.napier.ac.uk/id/eprint/9233
• Publisher URL: http://dx.doi.org/10.1371/journal.pone.0132113