High levels of testosterone inhibit ovarian follicle development by repressing the FSH signaling pathway / 华中科技大学学报（医学）（英德文版）

The effect of high concentrations of testosterone on ovarian follicle development was investigated. Primary follicles and granulosa cells were cultured in vitro in media supplemented with a testosterone concentration gradient. The combined effects of testosterone and follicle-stimulating hormone (FSH) on follicular growth and granulosa cell gonadotropin receptor mRNA expression were also investigated. Follicle growth in the presence of high testosterone concentrations was promoted at early stages (days 1-7), but inhibited at later stage (days 7-14) of in vitro culture. Interestingly, testosterone-induced follicle development arrest was rescued by treatment with high concentrations of FSH (400 mIU/mL). In addition, in cultured granulosa cells, high testosterone concentrations induced cell proliferation, and increased the mRNA expression level of FSH receptor (FSHR), and luteinized hormone/choriogonadotropin receptor. It was concluded that high concentrations of testosterone inhibited follicle development, most likely through regulation of the FSH signaling pathway, although independently from FSHR downregulation. These findings are an important step in further understanding the pathogenesis of polycystic ovary syndrome.

Altura final em criancas com puberdade precoce central: a experiência de um serviço de referência / Final Height in Children with Central Precocious Puberty the experience of a Specialized Center The Experience of a Specialized Center

Introdução: A puberdade precoce central ocorre principalmente devido a ativação precoce do eixo hipotalâmico-hipofisário-gonadal e conseqüentemente ao aumento do hormônios gonadotróficos. A prematura ativação desse eixo não envolve apenas mudanças físicas precoces da puberdade, mas também aceleração do crescimento linear e aceleração da maturação óssea, que leva a fusão das epífises ósseas de maneira prematura e à diminuição da altura final. Objetivo: Identificar a altura final de pacientes que apresentaram Puberdade Precoce Central atendidos no Serviço de Endocrinologia Pediátrica do Hospital Infantil Joana de Gusmão. Métodos: Foram avaliados os registros de pacientes que haviam atingido a AF no período de 1997-2007. As variáveis analisadas foram: sexo, idade cronológica, idade óssea, idade ao diagnóstico, idade ao atingir a altura final, tempo de tratamento até altura final, tempo de acompanhamento até a altura final, tratamento utilizado, altura no início e término do tratamento, altura predita pelo método de Bayley – Pinneau, altura-alvo e altura final ( transformada em escore z). Resultados: Foram incluídos 56 pacientes, 96,4 % do sexo feminino e 90,75 % dos pacientes apresentavam PPC idiopática. Os pacientes masculinos foram tratados com análogo do hormônio liberador de gonadotrofinas por 2,7 anos em média, enquanto que as pacientes femininas foram tratadas durante 3,1 anos. A altura final foi alcançada aos 15,1 anos nos meninos e 14,2 anos nas meninas.Conclusões: A média de altura final foi 171,25 cm no sexo masculino e 160,77 cm no sexo feminino. O escore-z de AF foi de -0,55 desvios padrão da média nos meninos e 0,04 desvios padrão da média nas meninas. A diferença entre altura final e altura alvo foi de -5,25 cm nos meninos e 2,4 cm nas meninas.

Background: Central precocious puberty is mainly due to the precocious activation of hypothalamic-pituitary-gonadal axis leading to an increase of gonadotropic hormones. The premature activation of this axis it involves not only early physical changes of puberty, but also linear growth acceleration and acceleration of bone maturation, which leads to early epiphyseal fusion and short adult height. Objective: To identify final height in central precocious puberty patients treated at Pediatric Endocrinology Service of Hospital Infantil Joana de Gusmão. Methods: The study evaluated the registration of patients that had reached the final height between 1997-2007. Data included sex, chronological age, bone age, age at diagnosis, age at final height, duration of treatment, duration of accompaniment from the start of treatment to final height, treatment used, height at the start and at the end of treatment, predicted height by Bayley – Pinneau method, target height and final height (these are transformed in z-score). Results: Fifty six patients were involved. 96,4 % were female sex and 90,75 % had idiopathic central precocious puberty. The males were treated with Gonadotropin Releasing Hormone Analogue by 2,7 years and females were treated by 3,1 years. Final height was reached at 15,1 years in boys and 14,2 years in girls. Conclusions: Final height average was 171,25 cm in males and 160,77 cm in females. The z-score of final height was -0,55 standard deviation of average in boys and 0,04 standard deviation of average in girls. The difference between final height and target height were -5,25 cm in boys and 2,4 cm in girls.

Síndrome da anovulação crônica: breve revisão / Chronic anovulation syndrome: a brief review

A síndrome de anovulação crônica caracteriza-se pela ausência persistente de ovulação. Manifesta-se, clinicamente, por amenorréia ou disfunção menstrual e pode surgir tanto na menarca como tardiamente. Esta síndrome pode ser conseqüência de defeitos do córtex cerebral-hipotálamo-hipófise, retroalimentação anômala ou disfunção endócrina periférica associada a alterações centrais. Pode ser classificada em primária e secundária. Em geral, as pacientes com anovulação crônica têm espanioamenorréia ou até amenorréia, infertilidade eHiperandrogenismo cutâneo (hirsutismo e acne), podem ser obesas. O tratamento deve ser individualizado para cada situação. Como medida primária, deve-se realizar controle nutricional, exercícios e aporte psicológico para as pacientes. Já o medicamentoso, baseia na sintomatologia da paciente. Nas pacientes que desejam a gestação, pode-se estimular a ovulação...

The Effects of Gonadotropins on the Development of Ovarian Cancer / 대한산부인과학회잡지

OBJECTIVE: We performed immunohistochemistry for the evaluation of follicle stimulating hormone receptor (FSHR), luteinizing hormone receptor (LHR) expression in the ovarian tumors and examined the blood level of the gonadotropins in ovarian cancer patients to investigate ovarian carcinogenesis process related to gonadotropins. METHODS: Between January 2002 and July 2003, 25 patients with ovarian tumors were treated in the Hallym University Sacred Heart Hospital. 25 ovarian tumors including 7 borderline tumors, 1 sex cord stromal tumor, 1 germ cell tumor, and 16 carcinomas were examined for FSHR, LHR expression by immunohistochemistry. Serum gonadotropins were collected from 13 cases of 25 ovarian tumors who were not taking hormones at the time of blood collection. RESULTS: Followings are results summarized. 1. Mean FSH levels were lower among cases compared with controls. LH levels were lower among cases than controls, but the difference was not statistically significant. 2. The steady decline of FSHR, LHR expression from borderline tumor (86%, 100%) to carcinoma (56%, 43%) is observed. 3. Patients showing significant gonadotropins receptors expression showed lower serum FSH and LH levels when compared with patients with no detectable gonadotropins receptors. CONCLUSION: The presence of FSHR, LHR in ovarian tumors provide additional evidence supporting the relation of gonadotropins and ovarian carcinogenesis. But, this study did not support the hypothesis that pituitary goandotropins increase the risk of ovarian cancer. The decline of receptor expression from borderline tumors to carcinoma suggests that FSH, LH may be needed in early ovarian cancer development. If further studies of gonadal peptides and gonadotropins are done, we can suggest the cut-off value of gonadotropins on ovarian carcinogenesis.

Cloning of partial putative gonadotropin hormone receptor sequence from fish.

A search for the presence of mariner-like elements in the Labeo rohita genome by polymerase chain reaction led to the amplification of a partial DNA sequence coding for a putative transmembrane domain of gonadotropin hormone receptor. The amplified DNA sequence shows a high degree of homology to the available turkey and human luteinizing and follicle stimulating hormone receptor coding sequences. This is the first report on cloning such sequences of piscine origin.

role of monoamines in the regulation of pituitary gonadotropins in normal and castrated rats

Despite suggestion of multiplicity of neurotransmitters and neuromodulators contributing in the regulation of pituitary gonadotropins secretion the picture regarding catecholamines in intact and castrated rats is not clear. This study deals with the differential response of pituitary FSH and LH to immediate effect of different adrenergic and non - adrenergic agonist/antagonist [adrenaline, noradrenaline, proparnolol, isoprenaline, clonidine, phenoxybanzamine HCI] in the short -term castrated rat model. The evidence is presented for a direct excitatory or facilitatory effect of adrenaline and noradrenaline for pituitary LH regulation viz - a viz testosteron feed back mechanism in castrated rats

Saturnism in the male rat: endocrine effects

The effect of exposure to lead on endocrine function was studied in pubertal rats treated with 1.0 g/l lead acetate (PbAc) in drinkin water for 20 days (subacute group) or 9 months (chronic group) in addition to iv injections of PbAc (0.1mg/100g body weight) every 10(subacute group) or 15 days (chronic group). Although basal levels of testosterone were higher both in the plasma and in the testes of acuctely intoxicated animals, the ciruclating levels of lutinizing hormone (LH) were not affected in either group, nor was the LHRH content of the median eminence. The density of [125I]LH/hCG biding sites in testicular homogenates was reduced by saturnism in both groups. Howeverm the apparent affinity constant of the hormone-receptor complex significantly increased. These data can be viewed as the result of a mixture of specific lead toxicity (e.g., at the enzyme level) with other more general actions (e.g., at the level of the hypothalamus-pituitary-testicular axis)