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Title: Hormonal Levels and Secretory Pattern in Rhesus Monkeys with Induced Polycystic Ovaries
Authors: Dr. M. Arslan
Issue Date: 27-Jun-1982
Publisher: Department of Biological Sciences, Quaid-i-Azam University Islamabad
Series/Report no.: PP-276;C-QU/Med(55)
Abstract: Polycystic ovaries are often encountered among women, cattle and laboratory mammals and are a common cause of abnormal reproductive cycle and infertility. It is generally recognized that the polycystic ovarian syndrome is the result of an imbalance in the hypothalamic-pituitary axis and may involve an impairment of the cyclicity of gonadotropin release. It has been possible to induce polycystic ovaries in small laboratory animals through different experimental procedures. Thus, administration of androgen to neonatal female rats results in infertility characterized by polycystic ovaries (Barraclough, 1961). A similar ovarian condition may also be induced in the rat by hypothyroidism and hCG (Leathem, 1958). Although the histological changes characteristic of the polycystic ovaries are well recognized, the aetiology and pathophysiology of this syndrome remain obscure. In the rat, the polycystic ovaries have been shown to exhibit a marked increase in secretion of androgens and oestrogens in response to LH (Weiz and Llod, 1965). Polycystic ovarian syndrome has also been induced in the rat as a result of chronic treatment with DHA (Ward et al. , 1978). In this study, LH levels were shown to depressed whereas FSH and Prolactin were elevated in animals with DHA induced ovarian Cysts. Surwilo and Doeg (1973) have been reported metabolic changes in oxygen and lactate production in polycystic rats ovaries. Incidence of cystic ovaries in cattle is generally ascribed to a deficiency of LH and increased secretion of FSH. Hormonal profiles in cattle with cystic ovaries indicate lower than in animals exhibiting normal oestrous cycle (Edqvist et al. , 1974). The reported changes in Hormone production in Plycystic ovarian syndrome in women, have been shown to be highly variable. In most cases concentrations of LH and androgens are generally raised, although they vary from one patient to another (Baird et al., 1977; Yen et al., 1976). Furthermore, an exaggerated response of LH to LH-RH has been observed in women with polycystic ovaries. Devane et al., (1975) demonstrates a significant elevation in basal LH, androstenedione and oestrone levels over that of controls. The polycystic ovarian syndrome is generally associated with an enhanced secretion of androgens by ovaries (Greenblatt and Mahesh, 1976). Erickson et al., (1979) have demonstrated a relatively low aromatase activity in the gransulosa cells from polycystic ovaries resulting in decreased oestrogen production by the follicle. Aono et al., (1977) have, however, reported that androgen levels in Japanese women with polycystic ovaries are relatively lower than those in patients in western countries. Previous experience in this laboratory has demonstrated that PMSG treatment induces an abnormal development of ovarian follicles, morphologically comparable, to polycystic ovarian condition. Little information is available regarding steroidogenic status of the ovarian tissue or pituitary-gonadal relationship in monkeys with experimentally induced cystic ovaries. In this investigation we have made an attempt to study changes in the ovarian morphology and plasma steroid levels accompanying chronic administration of PMSG to immature and adult monkeys. We hope that the present study will provide a convenient experimental model for a more detailed study of the endocrine imbalance accompanying polycystic ovarian syndrome in the human.
URI: http://142.54.178.187:9060/xmlui/handle/123456789/12588
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