Prenatal Testosterone Exposure Disrupts Insulin Secretion and Promotes Insulin Resistance
Open accessAbstract
Hyperandrogenemia and metabolic disturbances during postnatal life are strongly linked both to polycystic ovary syndrome and other conditions that arise from prenatal exposure to androgen excess. In an animal model of this condition, we reported that insulin sensitivity (IS) was lower in young female sheep born to testosterone-treated mothers versus sheep born to non-exposed mothers (control). This lower insulin sensitivity remains throughout reproductive life. However, it is unknown whether abnormal postnatal levels of testosterone (T) further decrease IS derived from prenatal exposure to testosterone. Therefore, we assessed the effects of an acute testosterone administration (40 mg) on IS and insulin secretion during an intravenous glucose tolerance test performed at 40 weeks of age (adulthood) in previously ovariectomized sheep at 26 weeks of age (prepuberty), that were either prenatally exposed to testosterone (T-females, n = 6) or not (C-females, n = 6). The incremental area under the curve of insulin was greater in C-females both with or without the acute testosterone treatment (P < 0.05). The ISI-Composite was lower after an acute testosterone treatment, only in T-females. We conclude that prenatal exposure to testosterone disrupts pancreatic insulin secretion in response to glucose and that in this setting further hyperandrogenemia may predispose to lower insulin sensitivity.
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Prenatal exposure to high levels of androgens can probably lead to the development of insulin resistance and PCOS.
“Moreover, prenatal exposure to high levels of androgens can probably lead to the development of IR and PCOS [53,54,55].”
From The Role of Glp-1 Receptor Agonists in Insulin Resistance with Concomitant Obesity Treatment in Polycystic Ovary Syndrome (2022) · cites this paper as [53]
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- Authors
- Carrasco, A., Recabarren, M. P., Rojas-García, P. P., Gutiérrez, M., Morales, K., Sir-Petermann, T., & Recabarren, S. E.
- Affiliations
- University of Concepción (CL)
- Corresponding author
- Carrasco, Albert
- Venue
- Scientific Reports
- Published
- 2020-01-15
- Volume
- 10
- Issue
- 1
- Pages
- 404-404
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6962362
- OpenAlex
- W3000197592
- Cited by
- 10
- References
- 36
- Citations by year
- 2025: 2 · 2023: 4 · 2022: 3 · 2021: 1
- FWCI
- 1.92
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Universidad de Chile (submittedVersion, cc-by-nc-nd)
- Funders
- Universidad de Concepción
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
- Keywords
- prenatal testosterone exposure, insulin secretion, insulin resistance, hyperandrogenemia, polycystic ovary syndrome, glucose tolerance test, insulin sensitivity index, pancreatic beta cells, hyperandrogenism
- MeSH terms
- Insulin Secretion, Animals, Female, Insulin Resistance, Pregnancy, Prenatal Exposure Delayed Effects, Sheep, Testosterone, Embryonic Development
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