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Prenatal Hyperandrogenization Induces Metabolic and Endocrine Alterations Which Depend on the Levels of Testosterone Exposure
TLDR
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
Fetal programming by androgen excess in rats affects ovarian fuel sensors and steroidogenesis
TLDR
It is concluded that androgen excess during prenatal life leads to developmental programming effects that affect ovarian fuel sensors and steroidogenesis in a phenotype-specific way. Expand
Prenatal hyperandrogenism induces alterations that affect liver lipid metabolism.
TLDR
It is concluded that prenatal hyperandrogenism generates both PHov and PHanov phenotypes with signs of liver alterations, imbalance in lipid metabolism and increased risk of developing metabolic syndrome. Expand
Prenatal hyperandrogenism and lipid profile during different age stages: an experimental study.
TLDR
It is demonstrated for the first time that abnormalities in PPAR-γ and lipid profile were higher in rats showing an anovulatory phenotype than those displaying an ovulatory phenotype, which reveals the importance of evaluating the complete lipid profile, especially at early stages of life after the prenatal hyperandrogenism condition. Expand
Uterine Function: From Normal to Polycystic Ovarian Syndrome Alterations.
TLDR
The present review describes the role of hormones, metabolites, cytokines, adhesion molecules and the insulin/glucose pathway related to the uterine endometrium in women with PCOS and their role in implantation failure and development of endometrial cancer. Expand
Metformin improves ovarian insulin signaling alterations caused by fetal programming.
TLDR
The results suggest that PHanov rats have a defective insulin action, partially restored with metformin, and PHiov rats had less severe alterations, and meetformin treatment was more effective in this phenotype. Expand
Effect of hyperandrogenism on ovarian function.
TLDR
When folliculogenesis was induced in a hyperandrogenic condition, the mRNA levels of the PPARγ co-repressor NCoR remained higher than in controls and the pro-inflammatory and pro-oxidant statuses were enhanced. Expand
Prenatally androgenized female rats develop uterine hyperplasia when adult
TLDR
It is found that prenatal exposure to androgen excess alters the morphology of the uteri that show a hyperplastic morphology with increased total uterine thickness as well as luminal epithelium thickness, with both enhanced and altered distribution of glands as compared with controls. Expand
Effects of in utero androgen excess and metformin treatment on hepatic functions
TLDR
It is shown, for the first time, that androgen excess in utero promotes hepatic dysfunctions and that metformin treatment is able to specifically reverse those hepatic alterations and sheds light on the possible mechanisms of met formin action. Expand
Treatment with the synthetic PPARG ligand pioglitazone ameliorates early ovarian alterations induced by dehydroepiandrosterone in prepubertal rats.
TLDR
The findings suggest that PPARG activation plays important roles in modulating early ovarian function, and highlight the importance of understanding the role(s) of PP ARG activation in the ovary, and the possible involvement in the treatment of ovarian pathologies, and/or the impact in regulating/improving fertility. Expand
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