Development of the Polycystic Ovarian Condition (PCO) in the Estradiol Valerate-Treated Rat

Brawer, James R.; Muñoz, M. Lopez; Farookhi, Riaz

doi:10.1095/biolreprod35.3.647

Cited by 185 publications

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“…Furthermore, increased production of VIP may underlie increased ovarian capacity of EV-treated rats to produce estradiol, in the face of reduced circulating levels of FSH (reported previously; Brawer et al 1986, Rosa-e-Silva et al 2003.…”

Section: Discussionmentioning

confidence: 94%

“…Rats were injected with 2 mg EV on day 60G5 of postnatal life and studied 60 days later. In previous studies, we have demonstrated that this mode of treatment leads to polycystic ovarian morphology, persistent estrus condition accompanied with increased circulating estradiol levels (Brawer et al 1986, and hypersecretion of androgens and estradiol from ovaries incubated in vitro (Brawer et al 1986, Barria et al 1993, Rosa-E-Silva et al 2003. Anovulation combined with hyperandrogenism and/or polycystic ovaries are features reflective of women with poly cystic ovary syndrome (PCOS) (Rotterdam consensus 2004).…”

Section: Animalsmentioning

confidence: 99%

“…Since granulosa cell compartment is also the site for VIP biosynthesis (Hulshof et al 1994) and the ovarian cysts seen in EV-treated rats have reduced granulosa cell layers (Brawer et al 1986, the similar intraovarian level of VIP in EV-treated and estrus rats may be reflective of increased innervation of the polycystic ovaries of the EV-treated rats. However, before establishing a role for VIP in the initiation of ovarian pathologies, detailed studies at individual follicle levels are required.…”

Section: Vip-and Ev-induced Polycystic Ovariesmentioning

confidence: 99%

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Participation of vasoactive intestinal polypeptide in ovarian steroids production during the rat estrous cycle and in the development of estradiol valerate-induced polycystic ovary

Parra

Fiedler²,

Luna³

et al. 2007

Reproduction

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Vasoactive intestinal polypeptide (VIP) stimulates estradiol and progesterone release from ovarian granulosa cells in vitro. Very little information is available as to the role VIP plays in the control of steroid secretion during reproductive cyclicity and in ovarian pathologies involving altered steroid secretion. In this study, we determined the involvement of VIP in regulating ovarian androgen and estradiol release during estrous cyclicity and estradiol valerate (EV)-induced polycystic ovarian development in rats. Our findings show that androgen and estradiol release from ovaries obtained during different stages of rat estrous cycle mimic cyclic changes in steroid release observed in vivo with maximal release occurring during late proestrus. VIP increased androgen release from ovaries of all cycle stages except late proestrus and estradiol release from all cycle stages. Increases in VIP-induced androgen and estradiol release were maximal at early proestrus. Inclusion of saturating concentrations of androstenedione increased magnitude of VIP-induced estradiol release at diestrus and estrus but not proestrus. Magnitude of VIP-induced androgen and estradiol release tended to be greater in the ovaries from EV-treated rats with polycystic ovary compared with estrous controls. At the tissue level, ovarian VIP concentration was cycle stage dependent with highest level seen in diestrus. Maximum concentration of VIP was found in EV-treated rats. Changes in VIP were inversely related to changes in ovarian nerve growth factor, a neuropeptide involved in ovarian androgen secretion. These results strongly suggest that intraovarian VIP participates in the control of estradiol secretion during the rat estrous cycle and possibly in the maintenance of increased ovarian estradiol secretory activity of EV-treated rats.

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Section: Discussionmentioning

confidence: 94%

Section: Animalsmentioning

confidence: 99%

Section: Vip-and Ev-induced Polycystic Ovariesmentioning

confidence: 99%

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Participation of vasoactive intestinal polypeptide in ovarian steroids production during the rat estrous cycle and in the development of estradiol valerate-induced polycystic ovary

Parra

Fiedler²,

Luna³

et al. 2007

Reproduction

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“…Thus mouse models are good and affordable choice for this purpose (9). Numerous experimental models for PCOM have been developed using EV (18). EV can produce a PCOM model in rat with interrupting in metabolic and physiologic processes (19).…”

Section: Body Weight and Fertility Ratementioning

confidence: 99%

Polycystic Ovary Morphology (PCOM) in Estradiol Valerate Treated Mouse Model

Amini¹,

Tehranian²,

Movahedin³

et al. 2016

IJWHR

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IntroductionPolycystic ovary syndrome (PCOS) is one of the most common endocrinopathies found among 5%-10% of reproductive age women. It is a common cause of infertility due to anovulatory (1) and hyperandrogenism (2). The name of PCOS is based on ovarian morphological changes in women who suffer from menstrual disturbances and hyperandrogenism symptoms, so polycystic ovary morphology (PCOM) can be a notable feature of PCOS (3). PCOM is revealed by some ovarian morphological abnormalities such as polycystic and enlarged ovaries (4). Although many extra ovarian causes are raised in the pathophysiology of PCOS, ovarian dysfunction plays the most important role in this field (5). Although all women with PCOS are in risk of hormonal and glucose metabolism disturbances, insulin resistance, dyslipidemia, metabolic syndrome, cardiovascular disease, and endometrial hyperplasia (4), it seems that PCOS women with PCOM are in risk of elevated serum DHEA-S levels and also taking a higher daily dose of insulin in comparison to PCOS women without PCOM (6).There are many hypotheses for the etiology of PCOS (7), but the exact initiating event in the pathophysiology of the syndrome is not entirely clear and remains poorly understood. Since the study of pathophysiology or any manipulation for treatment of PCOS/PCOM in human faces some serious logistic and ethical limitations; animal modeling is a good choice to improve the understanding of the abstruse aspects of PCOS (8). Since the 1960s, many animal models such as rodents, sheep and nonhuman primates have been applied for this purpose. Using the mouse models can provide an all-purpose tool for studying and understanding the comprehensive biologic mechanisms of PCOS/PCOM. They have stable genetic backgrounds, shorter reproductive and estrous cycle and generation times, and reasonably priced. Besides, these models have shown same reproductive and metabolic conditions as human PCOS (9). Different procedures have been suggested to produce PCOS model including prenatal or pre-pubertal androgen exposure (10,11), aromatase inhibitor or estradiol administration (11-13), and transgenic models (11). AbstractObjectives: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. Polycystic ovary (PCO) is a criterion for PCOS. Several animal models of polycystic ovary morphology (PCOM) are developed in order to study PCOS aspects. The present study aimed to develop a polycystic ovarian model in mice. Materials and Methods: Thirty-four young adult female mice were divided equally into estradiol valerate (EV) treated and control groups. Mice in experimental group (n = 18) received a single dose injection of EV (IM, 4 mg/kg). Weight and fertility rate of all mice were recorded. Morphology of ovarian follicles was assessed too. Chi-square and independent t test were used for comparison between groups. P value less than 0.05 was considered as significant level. Results: After 60 days, the weight of EV-treated mice was significantly lower than control (P ...

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“…Introduction Follicular cysts have been reported in many mammalian species, including cattle (Roberts 1971, Kesler & Garverick 1982, swine (Heinonen et al 1998), dogs (Arbeiter 1993, rabbits (Lopez-Bejar et al 1998), rats (Brawer et al 1986), mares (McCue & Squires 2002), sheep (Christman et al 2000), elephants (Brown et al 1999) and women (Stein & Leventhal 1935). In cattle, this condition is characterized by large (generally $25 mm in diameter) anovular structures that persist on the ovary for at least 10 days in the absence of a corpus luteum (CL) (Roberts 1971).…”

Section: Reproduction (2005) 129 737-745mentioning

confidence: 99%

Follicular cysts occur after a normal estradiol-induced GnRH/LH surge if the corpus hemorrhagicum is removed

Gümen

Wiltbank²

2005

Reproduction

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The pathophysiology underlying follicular cysts appears to be lack of an estradiol (E 2 )-induced GnRH/LH surge due to hypothalamic insensitivity to E 2 . In addition, progesterone (P 4 ) can cause animals with follicular cysts to resume normal cyclicity and normal hypothalamic responsiveness to E 2 . We postulated that follicular cysts may be a pathological manifestation of a physiological state that cows, and possibly other species, go through during the normal estrous cycle but the rise in P 4 following ovulation induces them back to normal hypothalamic responsiveness to E 2 . Based on this hypothesis, we expected that removal of the ovary containing the corpus hemorrhagicum would prevent the normal rise in P 4 following ovulation and induce development of follicular cysts. Cows (n 5 24) on day 7 of the estrous cycle were treated with prostaglandin F 2a (PGF 2a ) and time of ovulation was detected by ovarian ultrasonography every 8 h. Immediately following detection of ovulation, cows were randomly but unequally assigned to have the ovary containing the corpus hemorrhagicum removed (TRT; n 5 16) or the ovary opposite to the corpus hemorrhagicum removed (CON; n 5 8). Cows were subsequently evaluated by daily ultrasound and blood sampling to determine follicular dynamics. Ovulation was detected at 93.7 6 4.5 h after PGF 2a injection. All CON cows had a normal estrous cycle length (22.0 6 0.6 days) after ovariectomy (OVX). Half of the TRT cows became anovular (TRT-ANO; n 5 8) after OVX with large anovular follicles developing on the ovary (maximal size, 25.4 6 1.4 mm; range, 20-32 mm). However, eight TRT cows ovulated (TRT-OV; n 5 8) 7.3 6 0.6 days after OVX. Control cows had a normal P 4 rise after ovulation. Removal of the newly formed corpus hemorrhagicum prevented the rise in circulating serum P 4 in TRT-ANO cows throughout the 25-day experimental period. The TRT-OV cows had a delayed increase in circulating P 4 but it was normal in relation to time of ovulation. Serum E 2 concentrations were similar among groups (TRT-OV, TRT-ANO and CON cows) until 7 days after OVX. Serum E 2 concentrations then decreased in TRT-OV and CON cows but remained elevated (> 5 pg/ml) in TRT-ANO cows. Thus, the endogenous increase in circulating E 2 that induces the GnRH/LH surge and estrus is sufficient to induce cows into a physiological state that resembles follicular cysts if it is not followed by increased circulating P 4 . Reproduction (2005) 129 737-745Introduction Follicular cysts have been reported in many mammalian species, including cattle (Roberts 1971, Kesler & Garverick 1982, swine (Heinonen et al. 1998), dogs (Arbeiter 1993, rabbits (Lopez-Bejar et al. 1998), rats (Brawer et al. 1986), mares (McCue & Squires 2002), sheep (Christman et al. 2000), elephants (Brown et al. 1999) and women (Stein & Leventhal 1935). In cattle, this condition is characterized by large (generally $25 mm in diameter) anovular structures that persist on the ovary for at least 10 days in the absence of a corpus luteum (CL) (Roberts 1...

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Development of the Polycystic Ovarian Condition (PCO) in the Estradiol Valerate-Treated Rat

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Cited by 185 publications

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Participation of vasoactive intestinal polypeptide in ovarian steroids production during the rat estrous cycle and in the development of estradiol valerate-induced polycystic ovary

Participation of vasoactive intestinal polypeptide in ovarian steroids production during the rat estrous cycle and in the development of estradiol valerate-induced polycystic ovary

Polycystic Ovary Morphology (PCOM) in Estradiol Valerate Treated Mouse Model

Follicular cysts occur after a normal estradiol-induced GnRH/LH surge if the corpus hemorrhagicum is removed

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