hyperandrogenism/sesamum indicum

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Prenatal hyperandrogenism and lipid profile during different age stages: an experimental study.

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OBJECTIVE The present study investigates the effect of prenatal hyperandrogenization on lipid metabolism and oxidant/antioxidant balance. METHODS Experimental study. METHODS Research institute. METHODS Pregnant Sprague Dawley rats were subcutaneously injected with 2 mg free T between days 16 and 19

Hyperandrogenism alters intraovarian parameters during early folliculogenesis in mice.

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This study aimed to investigate how hyperandrogenism affects early folliculogenesis. Hyperandrogenism was induced in prepuberal female BALB/c mice by daily s.c. injection of dehydroepiandrosterone (60 mg/kg body weight in 0.1 ml sesame oil) for 10 consecutive days. Although hyperandrogenism

Hyperandrogenism Induces Histo-Architectural Changes in the Rat Uterus.

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The effects of androgens on the uterus have been poorly studied and they need to be clarified to understand why androgen excess, such as observed in women with polycystic ovary syndrome (PCOS), is a risk factor for the development of endometrial hyperplasia, cancer, and infertility. Thus, uterine

Depression-Like Behavior in a Dehydroepiandrosterone-Induced Mouse Model of Polycystic Ovary Syndrome.

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Patients with polycystic ovary syndrome (PCOS) can suffer from psychological disorders, among which depression is the most commonly diagnosed. However, the pathogenesis is still unclear. The aims of the present study were to investigate the behaviors of dehydroepiandrosterone (DHEA)-induced PCOS

Ultra-low Doses of Follicle Stimulating Hormone and Progesterone Attenuate the Severity of Polycystic Ovary Syndrome Features in a Hyperandrogenized Mouse Model.

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BACKGROUND Polycystic-ovary syndrome (PCOS) is a reproductive illness characterized by hyperandrogenism and anovulation. Using hyperandrogenized mice, it was demonstrated that the oral administration of incremental dose of follicle stimulating hormone (FSH) attenuated some of PCOS characteristics.

The mechanism of mTOR (mammalian target of rapamycin) in a mouse model of polycystic ovary syndrome (PCOS).

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Polycystic ovary syndrome (PCOS) is a common and complex endocrine disorder affecting 5-10% of women in reproductive age that is characterized by hyperandrogenism, oligo- or anovulation and infertility. However the pathophysiology of PCOS still remains unknown. The mammalian target of rapamycin

Long-term treatment with dehydroepiandrosterone may lead to follicular atresia through interaction with anti-Mullerian hormone.

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BACKGROUND Hyperandrogenism is the primary manifestation of polycystic ovary syndrome (PCOS), which appears to be caused by excess exposure to androgen. As such, androgenized animal models have been developed and investigated to study the etiology of PCOS. Anti-Mullerian hormone (AMH) is known to be

Deficiency of Gpr1 improves steroid hormone abnormality in hyperandrogenized mice.

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BACKGROUND Polycystic ovary syndrome (PCOS) is a complex genetic disease with multifarious phenotypes. Many researches use dehydroepiandrosterone (DHEA) to induce PCOS in pubertal mouse models. The aim of this study was to investigate the role of GPR1 in dehydroepiandrosterone (DHEA)-induced

Assessment of PGC1α-FNDC5 Axis in Granulosa Cells of PCOS Mouse Model.

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UNASSIGNED Polycystic ovarian syndrome (PCOS) is a metabolic and endocrine disorder which is characterized by hyperandrogenism, anovulation or oligomenorrhea and polycystic ovarian morphology. It is believed that modulation in metabolism of granulosa cells of PCOS patients may lead to infertility.

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