Animal models of the polycystic ovary syndrome phenotype (original) (raw)

Rodent Models of Polycystic Ovary Syndrome: Phenotypic Presentation, Pathophysiology, and the Effects of Different Interventions

Seminars in Reproductive Medicine, 2014

Polycystic ovary syndrome (PCOS) is the most common endocrine and metabolic disorder affecting women of reproductive age. 1 Endocrine and reproductive symptoms of PCOS are hyperandrogenism (hirsutism, acne, and alopecia), irregular menstrual cycles, subfertility, and polycystic ovary morphology. Women with PCOS also tend to suffer from insulin resistance with compensatory hyperinsulinemia, type 2 diabetes, and cardiovascular disease, 2,3 but these symptoms is not part of the PCOS diagnosis. Obesity worsens all reproductive and metabolic symptoms of PCOS 4 and demonstrates the importance of prevention and treatment of obesity in women with PCOS. Women with PCOS also often suffer from symptoms of anxiety and depression that lead to reduced healthrelated quality of life.

A REVIEW AND A CRITICAL INTERPRETATION ON ANIMAL EXPERIMENTAL MODELS TO ANALYSE POLYCYSTIC OVARIAN DISEASE (PCOS

International Journal of Emerging Technologies and Innovative Research, 2022

PCOS is identified as most common endocrinal disorder affecting reproductive span of women's life. PCOS is burden on social life, medical systems and also its economical drain. This data gives more focus in research fields also, basically to study any disease some pathways is need to define. In the form of preclinical study and the clinical studies. Animal studies plays an important role to study the pathophysiology of any disease due to its mimic systems like human. PCOS is also being studied with the help of various animals. To study PCOS, common animal models of mice, rhesus monkeys, rats and ewes are used, induced with the route of subcutaneous injection or implantation of androgens, anti-progesterone, estrogens, and letrozole, prenatal coverage to excess androgens and by exposure to constant light. (1-6) MATERIAL-Various scientific research and review articles published in last 10 years were identified through pubmed and Google scholar websites using MeSH terms regarding the animal models of PCOS. With the combination of PCOS, all these key words were used to specify the pointed results: animal model, sheep, rodent, mouse, rat and fish. METHODOLOGY-Animal experimental models for PCOS are searched from more than 150 research articles and the review papers. These articles were grouped according to similar activity and the working mechanism and compiled accordingly. RESULTS AND DISCUSSION Etiology of PCOS is still exactly not unrevealed, but many of the survey studies mentions some major causing factors are sedentary life style, hormonal imbalance, genetic factors, environmental factors and some unknown factors. Considering all the events probable animal's models are generated. Most commonly used animals models according to major causative factors of PCOS are demonstrated in fig 1.

Rat Models of Polycystic Ovary Syndrome

Sourcebook of Models for Biomedical Research, 2008

Polycystic ovary (PCO) syndrome is a common endocrine disorder of unknown etiology. This condition is a major cause of menstrual irregularity and infertility in women with chronic anovulation. This chapter reviews the literature on methods of producing experimental PCO models in the laboratory rat, and the fi ndings that support their resemblance to the human condition. The principal rat PCO models that have been validated include constant light exposure, hypothalamic lesions, sex steroid-induced models, and the mifepristone (RU486) model. The biological systems involved in developing chronic anovulation and PCO in these models include the hypothalamus, the pituitary gland, the adrenals, and the ovary with its paracrine, autocrine, and intracrine regulators. Animal models are central to making the transition from scientifi c concepts to understanding the reality of a human disease. Validated animal models can be used for therapeutic screens, in preclinical trials, and for basic research in reproductive biology. However, animal models of chronic anovulation and PCO may not fully reproduce the reproductive events seen in the human syndrome.

Induction by Estradiol-17β of Polycystic Ovaries in the Guinea Pig1

Biology of Reproduction, 1993

In the present study we wished to develop a model for polycystic ovarian syndrome (PCOS) using the guinea pig, because this animal's cycle, compared to other rodent models, more closely emulates that of humans. Four silastic capsules, either empty or containing cholesterol or estradiol-17, were placed subcutaneously for 48 h on Day 10 or 12 of the cycle. Vaginal smears were taken daily. Cardiac blood was drawn at various intervals. At necropsy, trunk blood was collected and ovaries were excised and analyzed histologically. Cycle length was extended over that in controls in animals treated with estradiol-170 (E,) on Day 12 of the cycle. Treatment with E, resulted in an increase in serum estrogen 2 h after capsule insertion. No changes were evident in progesterone or androstenedione concentrations with treatment. Animals treated with E, and killed late (54 days after capsule removal) showed cysts grossly (group A), while occult cysts were present in E,-treated animals killed early (17 days; group B); no cysts were observed in control groups. Ovarian weight and size were increased in group A over controls. There was an increase in the fraction of atretic:total follicles < 500 mm in size in group A compared to group B as well as compared to controls. Since these results are similar to those seen in human PCOS, we conclude that the guinea pig may serve as an exceptional and unique model for the study of PCOS and may be applicable to humans.

Characterization of Reproductive, Metabolic, and Endocrine Features of Polycystic Ovary Syndrome in Female Hyperandrogenic Mouse Models

Endocrinology, 2014

Polycystic ovary syndrome (PCOS) affects 5–10% of women of reproductive age, causing a range of reproductive, metabolic and endocrine defects including anovulation, infertility, hyperandrogenism, obesity, hyperinsulinism, and an increased risk of type 2 diabetes and cardiovascular disease. Hyperandrogenism is the most consistent feature of PCOS, but its etiology remains unknown, and ethical and logistic constraints limit definitive experimentation in humans to determine mechanisms involved. In this study, we provide the first comprehensive characterization of reproductive, endocrine, and metabolic PCOS traits in 4 distinct murine models of hyperandrogenism, comprising prenatal dihydrotestosterone (DHT, potent nonaromatizable androgen) treatment during days 16–18 of gestation, or long-term treatment (90 days from 21 days of age) with DHT, dehydroepiandrosterone (DHEA), or letrozole (aromatase inhibitor). Prenatal DHT-treated mature mice exhibited irregular estrous cycles, oligo-ovula...

Polycystic ovary syndrome: pathogenetic mechanisms of the disease (part 1)

Siberian Medical Review

The article presents analysis of modern literature data on risk factors and pathogenesis of polycystic ovary syndrome (PCOS). Despite numerous studies, it has not been possible so far to formulate a unified concept of the pathogenesis and etiology of PCOS. This lecture considers mechanisms of PCOS development. The role of impaired steroidogenesis in the adrenal glands and ovaries in PCOS is observed. The focus is assigned to insulin resistance that is likely involved in the development of reproductive PCOS phenotype and might mediate on some of the changes in ovarian morphology seen in this disease. It has been shown that not only hereditary factors lead to the development of this syndrome, but also lifestyle, physical activity and concomitant somatic diseases.

Animal Models for the Study of Polycystic Ovarian Syndrome

Endocrinology and …, 2011

Corresponding author: CheMyong Ko. Department of Comparative Biosciences, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, 2001 South Lincoln Avenue, Urbana, IL 61802, USA. Tel: 217-333-9362, Fax: 217-244-1652, Email: jayko@ ...