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

Yaba, Aylin; Demır, Necdet

doi:10.1186/1757-2215-5-38

Cited by 53 publications

(42 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Despite the lack of significant differences between the two groups regarding preantral and antral follicles, similar to other studies (14,20,21), the preovulatory follicle and corpora lutea were significantly lower in EV-treated mice. This can be related to the reduced ovulatory rate or anovulation, explaining the poor fertility rate in this group.…”

Section: Body Weight and Fertility Ratesupporting

confidence: 71%

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

Amini¹,

Tehranian²,

Movahedin³

et al. 2016

IJWHR

View full text Add to dashboard Cite

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 ...

show abstract

Section: Body Weight and Fertility Ratesupporting

confidence: 71%

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

Amini¹,

Tehranian²,

Movahedin³

et al. 2016

IJWHR

View full text Add to dashboard Cite

show abstract

“…It is interesting to note that HFD-induced obesity accelerates the ovarian follicular development and the rate of follicle loss through activating mTOR signaling in rats [234]. mTOR has also recently been indicated to function in the PCOS mouse ovary [235]. However, whether these metabolic pathways in oocytes mediate the nutritional effects on pregnancy outcomes remains unknown.…”

Section: Methodsmentioning

confidence: 99%

Metabolic control of oocyte development: linking maternal nutrition and reproductive outcomes

Liu

Gu³

et al. 2014

Cell. Mol. Life Sci.

147

102

View full text Add to dashboard Cite

Obesity, diabetes, and related metabolic disorders are major health issues worldwide. As the epidemic of metabolic disorders continues, the associated medical comorbidities, including the detrimental impact on reproduction, increase as well. Emerging evidence suggests that the effects of maternal nutrition on reproductive outcomes are likely to be mediated, at least in part, by oocyte metabolism. Well-balanced and timed energy metabolism is critical for optimal development of oocytes. To date, much of our understanding of oocyte metabolism comes from the effects of extrinsic nutrients on oocyte maturation. In contrast, intrinsic regulation of oocyte development by metabolic enzymes, intracellular mediators, and transport systems is less characterized. Specifically, decreased acid transport proteins levels, increased glucose/lipid content and elevated reactive oxygen species in oocytes have been implicated in meiotic defects, organelle dysfunction and epigenetic alteration. Therefore, metabolic disturbances in oocytes may contribute to the diminished reproductive potential experienced by women with metabolic disorders. In-depth research is needed to further explore the underlying mechanisms. This review also discusses several approaches for metabolic analysis. Metabolomic profiling of oocytes, the surrounding granulosa cells, and follicular fluid will uncover the metabolic networks regulating oocyte development, potentially leading to the identification of oocyte quality markers and prevention of reproductive disease and poor outcomes in offspring.

show abstract

“…3,43,44 In the present study, we induced PCOS mice model by DHEA to mimic the human anovulatory PCOS and investigated the mechanism of action of vitamin D3 on steroidogenesis process in granulosa cells of the polycystic ovary. 1 In a previous study, we showed that steroidogenic key enzymes including Cyp11a1, Cyp19a1, 3βHSD, and StAR were upregulated in granulosa cells of polycystic ovaries in DHEA-treated mice. Also, we detected no corpus lutea in polycystic ovaries that confirmed disturbed folliculogenesis and failure in ovulation.…”

Section: Discussionmentioning

confidence: 86%

“…1 We also provided vehicle group by injecting 0.09-mL sesame oil (Sigma, USA) and 0.01-mL 95% ethanol (Merck, Germany) daily for 20 consecutive days and also control group without any treatment. 1 We also provided vehicle group by injecting 0.09-mL sesame oil (Sigma, USA) and 0.01-mL 95% ethanol (Merck, Germany) daily for 20 consecutive days and also control group without any treatment.…”

Section: Pcos Experimental Animal Model and Morphological Assessmentsmentioning

confidence: 99%

“…1 The specific clinical features of PCOS include clinical or biochemical hyperandrogenism, oligomenorrhea, or amenorrhea and polycystic ovarian morphology that could cause chronic anovulation and infertility. 1 The specific clinical features of PCOS include clinical or biochemical hyperandrogenism, oligomenorrhea, or amenorrhea and polycystic ovarian morphology that could cause chronic anovulation and infertility.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Vitamin D3 regulates steroidogenesis in granulosa cells through AMP‐activated protein kinase (AMPK) activation in a mouse model of polycystic ovary syndrome

Bakhshalizadeh

Amidi

Shirazi

et al. 2018

Cell Biochemistry & Function

View full text Add to dashboard Cite

Polycystic ovarian syndrome (PCOS) is an endocrine disorder of women in reproductive age. This disorder is partly related to disruption in steroidogenesis pathway and dysregulation of estradiol and progesterone production in granulosa cells of polycystic ovaries. Previously, we have shown that vitamin D3 could modulate steroidogenesis pathway in PCOS granulosa cells. In this study, we investigate the molecular mechanism of vitamin D3 in regulation of steroidogenesis pathway. We have shown that vitamin D3 has a modulating role in steroidogenesis pathway of granulosa cells by regulation of AMP-activated protein kinase (AMPK) as an underlying molecular mechanism in mouse polycystic ovary.

show abstract

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

Cited by 53 publications

References 48 publications

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

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

Metabolic control of oocyte development: linking maternal nutrition and reproductive outcomes

Vitamin D3 regulates steroidogenesis in granulosa cells through AMP‐activated protein kinase (AMPK) activation in a mouse model of polycystic ovary syndrome

Contact Info

Product

Resources

About