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Endocrine Abstracts (2014) 35 S25.3 | DOI: 10.1530/endoabs.35.S25.3

ECE2014 Symposia Gonadal hormones and obesity (3 abstracts)

Perinatal androgen exposure and body weight fate

Elisabet Stener-Victorin


Department of Physiology, Institute of Neuroscience and Physiology, Göteborg, Sweden.


The etiology of PCOS is not well understood, but genetic, epigenetic, and environmental factors have all been implicated in its development. Clinical evidence suggests that excessive secretion of sex steroids, in particular androgens, plays a role in the pathophysiology of PCOS. The main metabolic phenotype is hyperinsulinemia and insulin resistance (IR). These often precede the development of type 2 diabetes mellitus (T2DM) and occur independently of body weight, although obesity worsens all symptoms. Pregnant women with PCOS tend to be obese, have increased circulating androgens, and be at increased risk of developing gestational diabetes and pre-eclampsia. They are also at risk for having either small-for-gestational-age or large-for-gestational-age infants suggesting that maternal androgen excess affects the offspring.

Animal PCOS models are needed when making the transition from scientific concepts to attaining an understanding of a human disease. A number of prenatal androgenized animal models have been developed in rodents, sheep, and non-human primates, and their offspring develop a PCOS-like phenotype. Since most women start to develop their PCOS symptoms during early puberty, at the same time as the androgens are starting to be produced, we have developed two models in which continuous dihydrotestosterone (DHT), a nonaromatizable androgen, or letrozole, a non-steroidal inhibitor of P450 aromatase are administered from pre-pubertal age in order to study the contribution of androgens on female rats at adult age as a conceivable PCOS model. Similarities and dissimilarities with human PCOS with focus on metabolic aberrations as well as advantage and disadvantage of different rodent models will be discussed.

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