Neuroendocrine consequences of androgen excess in female rodents

Foecking, Eileen M.; McDevitt, Melissa A.; Acosta-Martínez, Maricedes; Horton, Teresa H.; Levine, Jon E.

doi:10.1016/j.yhbeh.2007.12.013

Cited by 67 publications

(53 citation statements)

References 196 publications

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“…This vicious cycle of androgen over-production pushed forward the pathogenesis of PCOS. Androgens have diverse roles in reproduction and affect brain development (Gao et al 2005, Foecking et al 2008. Previous studies have shown that long-term androgen treatment upregulated AR mRNA expression in the hypothalamus and further affected the activities of the hypothalamus-pituitaryovarian axis (Feng et al 2010).…”

Section: Discussionmentioning

confidence: 99%

High-fat diets exaggerate endocrine and metabolic phenotypes in a rat model of DHEA-induced PCOS

Zhang¹,

Yi²,

Zhang³

et al. 2016

Reproduction

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Polycystic ovary syndrome (PCOS) is a complex endocrine and metabolic disorder with unclear etiology and unsatisfactory management. Effects of diets on the phenotype of PCOS were not fully understood. In the present study, we applied 45 and 60% high-fat diets (HFDs) on a rat model of PCOS induced by postnatal DHEA injection. We found that both DHEA and DHEACHFDs rats exhibited reproductive abnormalities, including hyperandrogenism, irregular cycles and polycystic ovaries. The addition of HFDs, especially 60% HFDs, exaggerated morphological changes of ovaries and a number of metabolic changes, including increased body weight and body fat content, impaired glucose tolerance and increased serum insulin levels. Results from qPCR showed that DHEA-induced increased expression of hypothalamic androgen receptor and LH receptor were reversed by the addition of 60% HFDs. In contrast, the ovarian expression of LH receptor and insulin receptor mRNA was upregulated only with the addition of 60% HFDs. These findings indicated that DHEA and DHEACHFDs might influence PCOS phenotypes through distinct mechanisms: DHEA affects the normal function of hypothalamus-pituitary-ovarian axis through LH, whereas the addition of HFDs exaggerated endocrine and metabolic dysfunction through ovarian responses to insulin-related mechanisms. We concluded that the addition of HFDs yielded distinct phenotypes of DHEA-induced PCOS and could be used for studies on both reproductive and metabolic features of the syndrome.

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Section: Discussionmentioning

confidence: 99%

High-fat diets exaggerate endocrine and metabolic phenotypes in a rat model of DHEA-induced PCOS

Zhang¹,

Yi²,

Zhang³

et al. 2016

Reproduction

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“…The polycystic ovary not only occurs in women but also in many animals. For example, prenatal, perinatal, or postnatal androgen exposure in monkeys, sheep, rats, and mice can prompt the development of many of the symptoms of PCOS [11]. Some scholars believe that rhesus monkeys are the most similar to humans in reproductive physiology.…”

Section: Animals and Hormone Treatmentmentioning

confidence: 99%

Endocrine Traits of Polycystic Ovary Syndrome in Prenatally Androgenized Female Sprague-Dawley Rats

et al. 2010

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Polycystic ovary syndrome (PCOS) is a common endocrine disorder found in 5-10% of reproductive-age women and 75-80% of anovulatory women. Characteristics of PCOS include amenorrhea/ oligomenorrhea, infertility, hyperinsulinemia from insulin resistance, leutinizing hormone (LH) hypersecretion and hyperandrogenism [1]. The etiology and pathophysiology of PCOS are not clear, so the treatments only scratch the surface of the problem and drugs are needed to ease the symptoms. Some scholars have considered that PCOS is a single autosomal dominant genetic disease [2,3] abstract. although hyperandrogenism is an important condition and is considered the possible pathogenesis behind polycystic ovary syndrome (PCOS), data supporting this is still scarce. We sought to determine whether or not prenatal androgen exposure leads to PCOS and the possible cellular mechanisms involved. To induce prenatal androgen exposure, pregnant rats were treated with daily subcutaneous injections of free testosterone (T) or dihydrotestosterone (dHT) from embryonic days 16 to 19, and their female offspring were studied as adults. The mRna expression of the progesterone receptor (PR) in the preoptic area (POa) hypothalamus was higher in the experimental groups than in the control group after ovariectomy and stimulation with estradiol benzoate. The levels of T, P, leutinizing hormone (LH), and estradiol were higher in the experimental groups than in the control groups. The frequency and magnitude of LH secretion was increased in experimental rats as compared with the control group. The anogenital distance of the experimental groups was prolonged and the nipple number was lower than that of the control group. almost all experimental rats had prolonged or irregular estrous cycles. The experimental groups had fewer corpus luteum and preovulatory follicles and more preantral follicles and antral follicles than the controls. Our findings are consistent with the hypothesis that excess androgen during the prenatal period may cause PCOS. additionally, we show that hyperandrogenic interference in the release of preovulatory LH surges is mediated by the suppressive effects of androgens on PR expression in POa-hypothalamic tissue.

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“…In the rat, the absence of positive feedback is caused by the organizational actions of testosterone during development, which sexually differentiates the surge system so that it cannot respond to E 2 under any circumstances. 286 In contrast, E 2 induced a robust LH surge in male monkeys that were castrated as adults 287 and in hypogonadal men. 288 Moreover, some male monkeys showed apparently normal ovarian cycles when the testes were replaced with an ovary, 289 while similar procedures in rats resulted in constant estrus.…”

Section: Physiological Control Systems and Governing Gonadal Functionmentioning

confidence: 93%

Neuroendocrine Control of Gonadotropin Secretion

Goodman

2015

Knobil and Neill's Physiology of Reproduction

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Neuroendocrine consequences of androgen excess in female rodents

Cited by 67 publications

References 196 publications

High-fat diets exaggerate endocrine and metabolic phenotypes in a rat model of DHEA-induced PCOS

High-fat diets exaggerate endocrine and metabolic phenotypes in a rat model of DHEA-induced PCOS

Endocrine Traits of Polycystic Ovary Syndrome in Prenatally Androgenized Female Sprague-Dawley Rats

Neuroendocrine Control of Gonadotropin Secretion

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