Fetal programming by androgen excess in rats affects ovarian fuel sensors and steroidogenesis

  title={Fetal programming by androgen excess in rats affects ovarian fuel sensors and steroidogenesis},
  author={G. A. Abruzzese and M. F. Heber and Fiorella Campo Verde Arbocc{\'o} and S. R. Ferreira and A. Motta},
  journal={Journal of Developmental Origins of Health and Disease},
  pages={645 - 658}
Abstract Fetal programming by androgen excess is hypothesized as one of the main factors contributing to the development of polycystic ovary syndrome (PCOS). PCOS is more than a reproductive disorder, as women with PCOS also show metabolic and other endocrine alterations. Since both ovarian and reproductive functions depend on energy balance, the alterations in metabolism may be related to reproductive alterations. The present study aimed to evaluate the effect of androgen excess during… Expand
Prenatal androgen exposure affects ovarian lipid metabolism and steroid biosynthesis in rats.
Prenatal androgen exposure affects reproductive functions and has been proposed as an underlying cause of polycystic ovary syndrome (PCOS). In this study, we aimed to investigate the impact ofExpand
Prenatal testosterone exposure induces insulin resistance, uterine oxidative stress and pro-inflammatory status in rats
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Circular RNA expression profiling in the fetal side of placenta from maternal polycystic ovary syndrome and circ_0023942 inhibits the proliferation of human ovarian granulosa cell
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A role for PPARG in the programming of ovarian disruptions by prenatal T excess is suggested, including a decrease in antral follicular adiponectin expression and a contributory role for adip onectin in follicular persistence and ovulatory failure. Expand
Prenatal Hyperandrogenization Induces Metabolic and Endocrine Alterations Which Depend on the Levels of Testosterone Exposure
The data show that the levels of testosterone prenatally injected modulate the uterine environment and that this, in turn, would be responsible for the endocrine and metabolic abnormalities and the phenotype of PCOS during the adult life. Expand
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It is demonstrated that maternal T treatment alters fetal ovarian steroidogenic gene and microRNA expression and implicate direct actions of estrogens in addition to androgens in the reprogramming of ovarian developmental trajectory leading up to adult reproductive pathologies. Expand
Maternal androgen excess reduces placental and fetal weights, increases placental steroidogenesis, and leads to long-term health effects in their female offspring.
It is demonstrated for the first time that prenatal testosterone exposure alters placental steroidogenesis and leads to dysregulation of lipid metabolism in their adult female offspring. Expand
Transient prenatal androgen exposure produces metabolic syndrome in adult female rats.
It is concluded that transient prenatal androgen exposure produces features of the metabolic syndrome in adult female rats, and dyslipidemia and hepatic steatosis appear to be mediated by PA-induced increases in adiposity, whereas hyperinsulinemia appears to be a direct result of PA. Expand
Developmental programming: postnatal estradiol modulation of prenatally organized reproductive neuroendocrine function in sheep.
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Prenatal androgen excess enhances stimulation of the GNRH pulse in pubertal female rats.
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The time of prenatal exposure to androgens may have a significant role in the development of PCOS, and increased prenatal androgen levels are associated with hormonal changes and morphological disorders of the reproductive system. Expand