[ study of LHRHA2 and dopamine antagonists on gonadotropin II level in Abramis Brama orientalis [BERG, 1905]]

Synthetic LHRHa or its superactive analogues stimulate GTH release. It shows an overlap in the biological activity of LHRHa and GnRH in many teleost species. The aim of the present study was to investigate the effects of LHRIIa[2]. Metocloprarnide and Chlorpromazine on HPG axis and plasma levels of GHT II. Luteinizing Hormone Releasing Hormone Analogue 2 [LHRHa[2]] [3 micro g/kg] with dopamine antagonis's [Metoclopramide. [5 mg/kg] and Chlorpromazine [10 mg/kg]] were injected via I.M to 64 female Bream [Abramis brama orientalis] [0.71371 +/- 0.026 kg, BW] through combined and solilary teeatments: Positive Control [saline]. Metoclopramide [5 mg/kg]. Chlorpromazine [10 mg/kg]. LHRHa[2] [3 micro g/kg]. Metoclopramide [5 mg/kg] + LHRHa[2] [3 micro g/kg], Chlorpromazine [10 mg/kg]+LHRHa[2] [3 micro g/kg]. Metoclopramide [5 mg/kg] + Chlorpromazine [10 mg/kg]+LHRHa[2] [3 micro g/kg] and Negative Control [intact]. Fishes were examined through primary bleeding. injection and secondary bleeding. The time interval between two bleeding step was 5h. The GTH 11 measurement was conducted on the basis of RIA. Results indicate that while LHRHa, and Metocloptamide could significantly increase the level of GTH II [p<0.05]. Chlorpromazine did not showed any significant impact on the increase of GTH II [p> 0.05]. Meanwhile, compared to the complex treatments the individual treatments have had relatively significant effects [p< 0.05]. All compounds showed a positive stimulation effect on the HPG axis and GTH 11 level in plasma

Eixos hormonais na obesidade: causa ou efeito? / Hormonal axes in obesity: cause or effect?

Diversas alterações endócrinas são descritas na obesidade. O eixo corticotrófico encontra-se hiper-responsivo, com maior depuração dos hormônios e nível de cortisol normal. A caracterização do pseudo-Cushing é importante. A leptina parece ser um hormônio permissivo para o desencadeamento da puberdade. Em adultos, as gonadotrofinas são normais, hiperandrogenismo e hiperestrogenismo são encontrados. Nas mulheres, a resistência insulínica é central no desenvolvimento da síndrome dos ovários policísticos (SOP), associada a hiperandrogenemia ovariana. Nos obesos, GH geralmente é baixo e IGF1 normal. A função tireoidiana é habitualmente normal nos obesos.

Several endocrine changes have been described in the obesity state. The corticotropic axis is hyperresponsive and there is enhancement of hormonal clearance, but cortisol levels are within the normal range. It is important to characterize a pseudo-Cushing in obesity. Leptin seems to be a permissive hormone for the beginning of puberty. In adults, gonadotropines are normal, and hyperandrogenism and hyperestrogenism are found. In women, insulin resistance has a central role in polycystic ovarian syndrome (POS), which is associated to ovarian hyperandrogenemia. In obese subjects, growth hormone (GH) is generally low and IGF1 is normal. Thyroid function is commonly normal in obese subjects.

Pathology of ovary, uterus, vagina and gonadotrophs of female mice fed on Zn-deficient diet.

Dietary Zn-deficiency in mature female mice for 6 weeks caused a retardation of ovarian growth characterized by lack of vesicular and Grafian follicles, degenerated corpus luteum, distorted cell membranes of granulosa cells with pycnotic nuclei, poor development of theca interna, inordinate accumulation of sudanophilic granules in theca interna and interstitial cells. The vagina and uterus did not exhibit cyclic changes in their cytoarchitecture as a result of the cessation of estrous cycle after 6 weeks of dietary treatment. They displayed wide spread degenerative changes in their myometrial and endometrial layers. The uterine glands appeared collapsed with little or no secretion. The vagina lacked cornification. Their gonadotrophs reacted positive to PAS, identical to the control group observed at diestrous stage. However, they did not display a negative reaction, characteristic of the gonadotrophs at estrous stage of the control group, examined even at an interval of 1 day for 6 days in succession. These results point towards the suspension of steroidogenesis inspite of intact gonadotrophs under Zn-deficiency condition.

Efeitos da dopamina sobre a secreçäo do hormônio liberador das gonadotrofinas de sinaptossomos hipotalâmicos da rata / Effects of dopamine on gonadotropin-releasing hormone secretion from hypothalamic sinaptosomes of rats

A dopamina (DA) é um neutrotransmissor existente em altas concentraçöes em terminaçöes nervosas na eminência média. Esses terminais estäo em estreita contigüidade com as terminaçöes que secretam o hormônio liberador das gonadotrofinas (LHRH). Seu papel é controverso pois alguns autores reivindicam um efeito excitatório enquanto que outros sugerem um papel inibitório para essa catecolamina. No presente experimento procuramos verificar a açäo da DA, em concentraçöes de 10-4 a 10-8M, sobre a liberaçäo de LHRH de terminaçöes nervosas isoladas (sinaptossomos) do hipotálamo de ratas. Esse estudo foi feito em cada uma das fases do ciclo estral. Verificou-se que a DA em baixas concentraçöes tem um efeito estimulador sobre a liberaçäo do LHRH, com um aumento de 55% no diestro, 43% no estro e no proestro näo teve efeito significante. Em altas concentraçöes ocorre um efeito inibidor, com uma reduçäo de 70% do LHRH liberado no proestro, 40% no estro e 34% no diestro. Esses resultados permitem sugerir que a discordância na literatura pode ocorrer pelo emprego de doses diferentes de DA e pelo uso de animais em diferentes fases do ciclo estral

Studies on the Mechanism of Post-partum Amenorrhea: Pituitary-Ovarian Axis during Post-partum Amenorrhea in Lactating Women

The aim of this study is to evaluate pituitary-ovarian function at different postpartum periods during the lactational amenorrhea in order to understand the mechanism by which puerperal lactation is associated with a protracted period of amenorrhea and natural infertility. Ninety four lactating women and 119 lactating women with menstruation, aged between 21 and 38 years, volunteered for this study. The pituitary was relatively insensitive to LH-RH during the first 3 weeks following delivery. The recovery of FSH responsiveness to LH-RH occurred earlier than that of LH. Normal FSH response resumed in the 2nd week while the LH response, although not normal, started at the 3rd week postpartum. Pituitary responsiveness after the 5th week postpartum was similar to that occurring in normally menstruating women, except that FSH response was exagerated. Serum prolactin levels were elevated above 160 ng/ml until the 5th week postpartum and decreased to 84.2 ng/ml in the 6th week postpartum. It appears that at least one reason for anovulation during the first four weeks following delivery is the relative insensitivity of the pituitary to hypothalamic stimulation. Prolactin does not seem to modulate pituitary responsiveness to LH-RH. In order to clarify hormonal profiles during the lactational amenorrhea beyond the 5th week puerperium, serum levels of LH, FSH, prolactin, estradiol and progesterone were determined during different postpartum periods. Serum FSH and LH levels during 1-10 months postpartum were similar to basal levels seen during the normal menstrual cycle. Serum estradiol concentrations throughout 1-10 months postpartum, however, were significantly decreased as compared with the levels during the follicular phase of the normal menstrual cycle. Serum prolactin levels were elevated throughout 1-10 months postpartum in lactating amenorrhic women but decreased as the postpartum period lengthened. As compared with lactating amenorrhic women, lactating women with resumed menstruation showed a decrease in prolactin levels from 89.20 ng/ml to 51.39 ng/ml at 1-3 months, from 75.08 ng/ml to 49.99 ng/ml at 4-6 months, and from 54.73 ng/ml to 28.74ng/ml at 7-10 months postpartum. These results suggest that the apparent anovulation seen beyond 5th week postpartum during lactation was not due to pituitary insensitivity to LH-RH. Rather, prolactindependent mechanism interfering with cyclic activity may be operative during long term lactation.