RESUMO
Several aspects of the physiology and behavior of organisms are expressed rhythmically with a 24-h periodicity and hence called circadian rhythms. Such rhythms are thought to be an adaptive response that allows to anticipate cyclic events in the environment. In mammals, the circadian system is a hierarchically organized net of endogenous oscillators driven by the hypothalamic suprachiasmatic nucleus (SCN). This system is synchronized by the environment throughout afferent pathways and in turn it organizes the activity of tissues by means of humoral secretions and neuronal projections. It has been shown that reproductive cycles are regulated by the circadian system. In rodents, the lesion of the SCN results on alterations of the estrous cycle, sexual behavior, tonic and phasic secretion of gonadotropin releasing hormone (GnRH)/gonadotropins and in the failure of ovulation. Most of the studies regarding the circadian control of reproduction, in particular of ovulation, have only focused on the participation of the SCN in the triggering of the proestrus surge of gonadotropins. Here we review aspects of the evolution and organization of the circadian system with particular focus on its relationship with the reproductive cycle of laboratory rodents. Experimental evidence of circadian control of neuroendocrine events indispensable for ovulation that occur prior to proestrus are discussed. In order to offer a working model of the circadian regulation of reproduction, its participation on aspects ranging from gamete production, neuroendocrine regulation, sexual behavior, mating coordination, pregnancy and deliver of the product should be assessed experimentally.
Assuntos
Ritmo Circadiano , Reprodução , Animais , Ciclo Estral , Feminino , Hormônio Liberador de Gonadotropina/metabolismo , Hormônio Liberador de Gonadotropina/fisiologia , Gonadotropinas/metabolismo , Gonadotropinas/fisiologia , Humanos , Mamíferos/fisiologia , Gravidez , Núcleo Supraquiasmático/fisiologiaRESUMO
Potamodromous teleosts that require migration to reproduce show dysfunctions that block ovulation and spawning while in captivity. To understand the physiological basis of these reproductive dysfunctions, follicle-stimulating hormone b subunit (fshb) and luteinizing hormone b subunit (lhb) gene expression analyses by real-time quantitative PCR, together with measurements of estradiol (E 2), 17α-hydroxyprogesterone (17α-OHP) and 17α,20ß-dihydroxy-4-pregnen-3-one (17α,20ß-DHP) levels, were carried out throughout the reproductive cycle of the potamodromous Salminus hilarii. The following reproductive stages were evaluated in captive and wild females: previtellogenic (PV), advanced maturation/mature (AM) and regression/spent (REG/SPENT). In the wild females, fshb expression decreased from the PV to the AM stage, and the opposite pattern was detected for E 2, which increased from the PV to the AM stage. fshb was expressed at lower levels in captive than in wild females, and this difference did not change during the reproductive cycle. lhb expression also increased from the PV to the AM stage in both groups, but the wild females at the AM and REG/SPENT stages showed higher lhb expression levels than the captive females. The concentrations of 17α-OHP did not change during the reproductive cycle, and the levels were higher in the captive than in the wild females at all reproductive stages. 17α,20ß-DHP levels did not change between wild and captive females. However, in captive females, the transition from PV to AM stage was followed by an increase in 17α,20ß-DHP levels. These data indicate that dysfunctions in the gonadotropins and steroids synthesis pathways cause the ovulation failure in captive S. hilarii.
Assuntos
Characidae/fisiologia , Hormônios Esteroides Gonadais/fisiologia , Gonadotropinas/fisiologia , Ovário/fisiopatologia , Ovulação , 17-alfa-Hidroxiprogesterona/sangue , Animais , Estradiol/sangue , Feminino , Hormônio Foliculoestimulante/fisiologia , Hidroxiprogesteronas/sangue , Hormônio Luteinizante/fisiologiaRESUMO
Impaired testicular function, i.e., hypogonadism, can result from a primary testicular disorder (hypergonadotropic) or occur secondary to hypothalamic-pituitary dysfunction (hypogonadotropic). Hypogonadotropic hypogonadism can be congenital or acquired. Congenital hypogonadotropic hypogonadism is divided into anosmic hypogonadotropic hypogonadism (Kallmann syndrome) and congenital normosmic isolated hypogonadotropic hypogonadism (idiopathic hypogonadotropic hypogonadism). The incidence of congenital hypogonadotropic hypogonadism is approximately 1-10:100,000 live births, and approximately 2/3 and 1/3 of cases are caused by Kallmann syndrome (KS) and idiopathic hypogonadotropic hypogonadism, respectively. Acquired hypogonadotropic hypogonadism can be caused by drugs, infiltrative or infectious pituitary lesions, hyperprolactinemia, encephalic trauma, pituitary/brain radiation, exhausting exercise, abusive alcohol or illicit drug intake, and systemic diseases such as hemochromatosis, sarcoidosis and histiocytosis X. The clinical characteristics of hypogonadotropic hypogonadism are androgen deficiency and a lack/delay/stop of pubertal sexual maturation. Low blood testosterone levels and low pituitary hormone levels confirm the hypogonadotropic hypogonadism diagnosis. A prolonged stimulated intravenous GnRH test can be useful. In Kallmann syndrome, cerebral MRI can show an anomalous morphology or even absence of the olfactory bulb. Therapy for hypogonadotropic hypogonadism depends on the patient's desire for future fertility. Hormone replacement with testosterone is the classic treatment for hypogonadism. Androgen replacement is indicated for men who already have children or have no desire to induce pregnancy, and testosterone therapy is used to reverse the symptoms and signs of hypogonadism. Conversely, GnRH or gonadotropin therapies are the best options for men wishing to have children. Hypogonadotropic hypogonadism is one of the rare conditions in which specific medical treatment can reverse infertility. When an unassisted pregnancy is not achieved, assisted reproductive techniques ranging from intrauterine insemination to in vitro fertilization to the acquisition of viable sperm from the ejaculate or directly from the testes through testicular sperm extraction or testicular microdissection can also be used, depending on the woman's potential for pregnancy and the quality and quantity of the sperm.
Assuntos
Hipogonadismo , Doenças do Sistema Endócrino/etiologia , Doenças do Sistema Endócrino/terapia , Gonadotropinas/fisiologia , Terapia de Reposição Hormonal/métodos , Humanos , Hipogonadismo/diagnóstico , Hipogonadismo/etiologia , Hipogonadismo/terapia , Infertilidade Masculina/etiologia , Infertilidade Masculina/terapia , Masculino , Resultado do TratamentoRESUMO
Impaired testicular function, i.e., hypogonadism, can result from a primary testicular disorder (hypergonadotropic) or occur secondary to hypothalamic-pituitary dysfunction (hypogonadotropic). Hypogonadotropic hypogonadism can be congenital or acquired. Congenital hypogonadotropic hypogonadism is divided into anosmic hypogonadotropic hypogonadism (Kallmann syndrome) and congenital normosmic isolated hypogonadotropic hypogonadism (idiopathic hypogonadotropic hypogonadism). The incidence of congenital hypogonadotropic hypogonadism is approximately 1-10:100,000 live births, and approximately 2/3 and 1/3 of cases are caused by Kallmann syndrome (KS) and idiopathic hypogonadotropic hypogonadism, respectively. Acquired hypogonadotropic hypogonadism can be caused by drugs, infiltrative or infectious pituitary lesions, hyperprolactinemia, encephalic trauma, pituitary/brain radiation, exhausting exercise, abusive alcohol or illicit drug intake, and systemic diseases such as hemochromatosis, sarcoidosis and histiocytosis X. The clinical characteristics of hypogonadotropic hypogonadism are androgen deficiency and a lack/delay/stop of pubertal sexual maturation. Low blood testosterone levels and low pituitary hormone levels confirm the hypogonadotropic hypogonadism diagnosis. A prolonged stimulated intravenous GnRH test can be useful. In Kallmann syndrome, cerebral MRI can show an anomalous morphology or even absence of the olfactory bulb. Therapy for hypogonadotropic hypogonadism depends on the patient's desire for future fertility. Hormone replacement with testosterone is the classic treatment for hypogonadism. Androgen replacement is indicated for men who already have children or have no desire to induce pregnancy, and testosterone therapy is used to reverse the symptoms and signs of hypogonadism. Conversely, GnRH or gonadotropin therapies are the best options for men wishing to have children. Hypogonadotropic hypogonadism is one of the rare conditions in which specific medical treatment can reverse infertility. When an unassisted pregnancy is not achieved, assisted reproductive techniques ranging from intrauterine insemination to in vitro fertilization to the acquisition of viable sperm from the ejaculate or directly from the testes through testicular sperm extraction or testicular microdissection can also be used, depending on the woman's potential for pregnancy and the quality and quantity of the sperm.
Assuntos
Humanos , Masculino , Hipogonadismo , Doenças do Sistema Endócrino/etiologia , Doenças do Sistema Endócrino/terapia , Gonadotropinas/fisiologia , Terapia de Reposição Hormonal/métodos , Hipogonadismo/diagnóstico , Hipogonadismo/etiologia , Hipogonadismo/terapia , Infertilidade Masculina/etiologia , Infertilidade Masculina/terapia , Resultado do TratamentoRESUMO
Cadherins are adhesion molecules that play a crucial role in tissue morphogenesis. Studies on N-cadherin and E-cadherin in the ovary of fetal hamster suggest that these adhesion molecules are involved in primordial follicle formation. In chicken embryo, present results demonstrate that N-cadherin is located on the surface epithelium and in the cortical cords of the ovary. Moreover, N-cadherin is identified in germ cells on day 14 of chicken embryo development. Quantification of mRNA of N-cadherin and E-cadherin demonstrates that treatments with follicle-stimulating hormone (FSH) or human chorionic gonadotropin (hCG), increase N-cadherin expression. Whereas, E-cadherin expression is decreased by gonadotropin treatments. The negative correlation between both cadherins expression is demonstrated after 18 h of hormonal treatment. Regulation of cadherin expression by gonadotropins and the presence of N-cadherin in the ovarian cortex suggest that these adhesion molecules are involved in ovarian morphogenesis in the chicken embryo.
Assuntos
Caderinas/genética , Embrião de Galinha/metabolismo , Gonadotropinas/fisiologia , Ovário/metabolismo , Animais , Caderinas/metabolismo , Células Cultivadas , Gonadotropina Coriônica/farmacologia , Feminino , Imunofluorescência , Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos , Gonadotropinas/farmacologia , Humanos , Morfogênese/efeitos dos fármacos , Morfogênese/genética , Morfogênese/fisiologia , Ovário/citologia , Ovário/efeitos dos fármacos , Ovário/embriologia , Cultura Primária de Células , Reação em Cadeia da Polimerase Via Transcriptase ReversaRESUMO
Ovarian function in dogs is minimally but successfully evolved and adapted for fertility, and represents a basic model for examining the more complex evolution of ovarian activity in other carnivores and mammals in general. Canids are monoestrous, polytocous, spontaneous ovulators with a spontaneous luteal function producing progesterone for the duration of a normal 2-month pregnancy and unaffected by hysterectomy. They have no acute luteolytic mechanism in the absence of pregnancy although PGF is luteolytic and participates in prepartum luteolysis. The cellular mechanisms of luteal and follicular tissues appear unlikely to differ meaningfully from those described in other species, with the spontaneously prolonged luteal function being similar to, and in some instances shorter than, the luteal lifespan of hysterectomized polyestrous species. All or nearly all female caniform carnivore species have photo-entrained annual life-cycles and annual or biennial reproduction. However, the domestic dog, a subspecies of the grey wolf, is an exception and non-seasonal; but, as an exception to the exception, the basenji dog like the dingo, another wolf subspecies, is seasonal, having its cycle in the autumn. The canine obligate anestrus lasts 2-10 months and is terminated by increased GnRH and LH pulsatility. The timing is under multiple regulatory inputs. These include recovery from progesterone effects at variable times after progesterone declines to nadir values; increased dopaminergic and/or decreased opioidergic tones and/or sensitivities, presumably under the influence of an endogenous circannual cycle assumed to persists despite the lack of photoresponsiveness; and, stimulatory pheromonal input from other females (as well as photoperiod in the case of Basenji). The only clear adaptations or unique attributes seen in dogs that are likely beyond what occurred in a more primitive ancestor are two. One, there is a pregnancy specific increase in prolactin that as a potent luteotrophin (as in rodents) acts to enhance progesterone production during pregnancy, which appears likely to be the case in all carnivores. And, two, the bitch has a fertile-mating window as wide as 11 days, and up to 8 days after ovulation. The latter involves the delayed post-ovulatory maturation of oocytes (also seen in foxes), prolonged post-maturation oocyte viability, and a uterine environment hospitable to sperm survival for up to 7 days during estrus. This relative simplicity contrasts to more complicated adaptive strategies like (1) delayed implantation seen in many caniform carnivores (including many mustelids, ursids, and phocid and otarid seals); (2) reflex, induced ovulation (as seen in many feliform carnivores); and (3) prolongation of post-implantation gestation via placental secretion of progesterone (some feliform, some artiodactyls, primates) or gonadotrophin (primates, equids). Also considered in the review are the endocrine mechanisms triggering the LH surge and estrus behavior in dogs, and factors involved in termination of obligate anestrus.(AU)
Assuntos
Animais , Gatos , Cães , Testes de Função Ovariana , Folículo Ovariano/crescimento & desenvolvimento , Ovário/fisiologia , Indução da Ovulação , Comportamento Sexual Animal/fisiologia , Corpo Lúteo/crescimento & desenvolvimento , Gonadotropinas/efeitos adversos , Prenhez/fisiologia , Anticoncepção/métodos , Ciclo Menstrual , Cães/fisiologia , Felidae/fisiologia , Anestro/fisiologia , Fertilização/fisiologia , Gonadotropinas/fisiologiaRESUMO
Ovarian function in dogs is minimally but successfully evolved and adapted for fertility, and represents a basic model for examining the more complex evolution of ovarian activity in other carnivores and mammals in general. Canids are monoestrous, polytocous, spontaneous ovulators with a spontaneous luteal function producing progesterone for the duration of a normal 2-month pregnancy and unaffected by hysterectomy. They have no acute luteolytic mechanism in the absence of pregnancy although PGF is luteolytic and participates in prepartum luteolysis. The cellular mechanisms of luteal and follicular tissues appear unlikely to differ meaningfully from those described in other species, with the spontaneously prolonged luteal function being similar to, and in some instances shorter than, the luteal lifespan of hysterectomized polyestrous species. All or nearly all female caniform carnivore species have photo-entrained annual life-cycles and annual or biennial reproduction. However, the domestic dog, a subspecies of the grey wolf, is an exception and non-seasonal; but, as an exception to the exception, the basenji dog like the dingo, another wolf subspecies, is seasonal, having its cycle in the autumn. The canine obligate anestrus lasts 2-10 months and is terminated by increased GnRH and LH pulsatility. The timing is under multiple regulatory inputs. These include recovery from progesterone effects at variable times after progesterone declines to nadir values; increased dopaminergic and/or decreased opioidergic tones and/or sensitivities, presumably under the influence of an endogenous circannual cycle assumed to persists despite the lack of photoresponsiveness; and, stimulatory pheromonal input from other females (as well as photoperiod in the case of Basenji). The only clear adaptations or unique attributes seen in dogs that are likely beyond what occurred in a more primitive ancestor are two. One, there is a pregnancy specific increase in prolactin that as a potent luteotrophin (as in rodents) acts to enhance progesterone production during pregnancy, which appears likely to be the case in all carnivores. And, two, the bitch has a fertile-mating window as wide as 11 days, and up to 8 days after ovulation. The latter involves the delayed post-ovulatory maturation of oocytes (also seen in foxes), prolonged post-maturation oocyte viability, and a uterine environment hospitable to sperm survival for up to 7 days during estrus. This relative simplicity contrasts to more complicated adaptive strategies like (1) delayed implantation seen in many caniform carnivores (including many mustelids, ursids, and phocid and otarid seals); (2) reflex, induced ovulation (as seen in many feliform carnivores); and (3) prolongation of post-implantation gestation via placental secretion of progesterone (some feliform, some artiodactyls, primates) or gonadotrophin (primates, equids). Also considered in the review are the endocrine mechanisms triggering the LH surge and estrus behavior in dogs, and factors involved in termination of obligate anestrus.
Assuntos
Animais , Gatos , Cães , Comportamento Sexual Animal/fisiologia , Corpo Lúteo/crescimento & desenvolvimento , Folículo Ovariano/crescimento & desenvolvimento , Gonadotropinas/efeitos adversos , Indução da Ovulação , Ovário/fisiologia , Prenhez/fisiologia , Testes de Função Ovariana , Anestro/fisiologia , Anticoncepção/métodos , Ciclo Menstrual , Cães/fisiologia , Felidae/fisiologia , Fertilização/fisiologia , Gonadotropinas/fisiologiaRESUMO
El síndrome de poliquistosis ovárica (SPCO) es una de las endocrinopatías más comunes que afecta a las mujeres en edad reproductiva, su expresión clínica comienza en edad perimenárquica y si bien fue descripto hace más de 70 años, hasta el presente, el(los) mecanismo(s) fisiopatológico(s) que lo origina(n) no se conoce(n) con certeza. Debido a la gran heterogeneidad en la expresión clínica y bioquímica que caracteriza al SPCO es probable que existan subgrupos de pacientes en las que sea posible identificar alguno de los mecanismos implicados en la patogenia como el responsable de los principales signos y síntomas observados. La presente revisión propone conocer en profundidad las anormalidades neuroendocrinas como uno de los principales componentes del síndrome. En nuestra experiencia, las adolescentes con SPCO presentan hipersecreción de LH (aumento de la masa de LH secretada por pulso, de la frecuencia de pulsos y de la tasa de producción), y un patrón desordenado de secreción de LH (mayores valores de ApEn) en relación a adolescentes eumenorreicas. Varias líneas de evidencia sugieren que uno de los mecanismos responsables de estos defectos es el aumento de frecuencia de secreción del GnRH. Las adolescentes con SPCO secretan moléculas de LH con mayor actividad biológica y mayor proporción de isoformas con punto isoeléctrico más alcalino que las adolescentes eumenorreicas. La preponderancia de isoformas más básicas y más bioactivas en estas pacientes se relaciona con elevados niveles séricos de 17-hidroxiprogesterona, androstenodiona (A) y testosterona (T). El aumento de la frecuencia de pulsos de GnRH y un microambiente hormonal caracterizado por exceso de andrógenos podrían conjuntamente promover la predominante secreción de este tipo de isoformas de LH. En ausencia de obesidad, las pacientes con SPCO presentan un incremento de la tasa de producción de GH y un patrón de secreción más ordenado (menores valores de ApEn, similar al patrón de secreción de GH observado en el varón adulto). La mayor secreción de GH podría potenciar la acción gonadotrófica sobre la esteroideogénesis ovárica. Analizando la sincronía entre pares de hormonas relacionadas mediante dos técnicas complementarias (cross ApEn y cross correlación) se demuestra que las adolescentes con SPCO presentan un deterioro en las asociaciones entre LH-andrógenos comparadas con las adolescentes eumenorreicas. El desacople de la secreción bihormonal (LH-A y LH-T) en adolescentes con SPCO es consistente con defectos en el control de la secreción ovárica de andrógenos dependiente de LH y con una alteración en el control negativo que ejercen los andrógenos sobre la secreción GnRH/LH. Estas alteraciones neuroendocrinas en la unidad GnRH/LH y andrógenos ováricos podrían promover el hiperandrogenismo y alterar la maduración folicular.
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among women in reproductive age, frequently begins during adolescence causing menstrual irregularity and hirsutism. Although described up more than seventy years ago, the primary pathophysiologic mechanisms underlying this disorder remain unknown.There is not a single etiologic factor that fully accounts for the spectrum of abnormalities in the PCOS. This review addresses current knowledge about the neuroendocrine abnormalities as a major component of the syndrome. From this perspective, adolescents with PCOS exhibit an accelerated frequency and/or higher amplitude of LH pulses, augmentation of secretory burst mass, and a more disorderly LH release (higher ApEn) than eumenorrheic adolescents. Several lines of evidence suggest that the mechanisms underlying the defects in LH secretion in PCOS include an increased frequency of GnRH secretion. These patients also show elevated in vitro LH bioactivity and a preponderance of basic LH isoforms, which correlate positively with elevated serum of 17-hydroxyprogesterone, androstenedione (A), and testosterone (T) concentrations. Heightened GnRH drive of gonadotropin secretion and steroid-permissive milieu appear to jointly promote elevated secretion of basic LH isoforms. Non obese adolescents with PCOS secrete GH at a higher rate and with more orderly patterns (resembling a male profile) than controls. Indeed, GH appears to act as a co-gonadotropin. When synchronicity of paired hormone profiles was appraised by two independent, but complementary, statistical tools (cross-entropy and cross correlation), concomitant uncoupling of the pairwise synchrony of LH - androgens was demonstrated in girls with PCOS. Asynchrony of LH-A and LH-T pairs further localizes a pathway defect to LH-dependent feedforward control of ovarian androgen secretion. These abnormalities are also consistent with altered androgen negative feed-back regulation of GnRH/LH output. These data suggest that in PCOS there are anomalies of signaling between GnRH/LH and ovarian androgens that promote hiperandrogenism and impaired follicle maturation.
Assuntos
Humanos , Feminino , Adolescente , Síndrome do Ovário Policístico/sangue , Síndrome do Ovário Policístico/diagnóstico por imagem , Gonadotropinas/fisiologia , Hormônio Liberador de Gonadotropina , Hiperandrogenismo , Gonadotropinas/efeitos adversos , Gonadotropinas/química , Hormônios/química , Distúrbios MenstruaisRESUMO
CONTEXT: Several factors can affect adult height (AH) of patients with gonadotropin-dependent precocious puberty (GDPP) treated with depot GnRH analogs. OBJECTIVE: Our objective was to determine factors influencing AH in patients with GDPP treated with depot GnRH analogs. PATIENTS: A total of 54 patients (45 girls) with GDPP treated with depot GnRH analog who reached AH was included in the study. DESIGN: Univariate and multivariate analyses of the factors potentially associated with AH were performed in all girls with GDPP. In addition, clinical features of the girls who attained target height (TH) range were compared with those who did not. Predicted height using Bayley and Pinneau tables was compared with attained AH. RESULTS: In girls the mean AH was 155.3 +/- 6.9 cm (-1.2 +/- 1 sd) with TH range achieved by 81% of this group. Multiple regression analysis revealed that the interval between chronological age at onset of puberty and at the start of GnRH analog therapy, height sd scores (SDSs) at the start and end of therapy, and TH explained 74% of AH variance. The predicted height at interruption of GnRH therapy, obtained from Bayley and Pinneau tables for average bone age, was more accurate than for advanced bone age in both sexes. In boys the mean AH was 170.6 +/- 9.2 cm (-1 +/- 1.3 SDS), whereas TH was achieved by 89% of this group. CONCLUSIONS: The major factors determining normal AH in girls with GDPP treated with depot GnRH analogs were shorter interval between the onset of puberty and start of therapy, higher height SDS at the start and end of therapy, and TH. Therefore, prompt depot GnRH analog therapy in properly selected patients with GDPP is critical to obtain normal AH.
Assuntos
Estatura , Hormônio Liberador de Gonadotropina/uso terapêutico , Gonadotropinas/fisiologia , Puberdade Precoce/tratamento farmacológico , Adolescente , Adulto , Criança , Pré-Escolar , Feminino , Gosserrelina/uso terapêutico , Humanos , Leuprolida/uso terapêutico , Hormônio Luteinizante/sangue , Masculino , Puberdade Precoce/fisiopatologia , Análise de Regressão , Pamoato de Triptorrelina/uso terapêuticoRESUMO
CONTEXT: gamma-Aminobutyric acid (GABA) is a dominant inhibitory neurotransmitter involved in the modulation of brain electric activity and puberty onset in primates. GABA inhibitory effects on GnRH neurons are mainly mediated by GABA-A receptor alpha1-subunit. OBJECTIVE: The objective of this study was to investigate functional mutations or polymorphisms of the GABA-A receptor alpha1-subunit gene (GABRA1) in girls with idiopathic gonadotropin-dependent precocious puberty (GDPP) with and without electroencephalographic (EEG) abnormalities. DESIGN: The entire coding region of GABRA1 was sequenced in all patients. Two known GABRA1 polymorphisms were investigated by GeneScan software analysis or enzymatic restriction. Seventy-three normal women were used as controls for genetic study. EEG tracings were recorded in 23 girls with GDPP and 17 girls with adequate pubertal development. SETTING: The study was performed at a university hospital. PATIENTS: Thirty-one girls from 28 unrelated families with idiopathic GDPP were studied. RESULTS: Automatic sequencing revealed no functional mutations in girls with GDPP. Seven different GABRA1 polymorphisms, including two exonic (156T>C and 1323G>A) and five intronic [IVS2-712(GT)n, IVS3+12A>T, IVS8+45T>G, IVS9+76A>G, and IVS10+15G>A], were found in GDPP girls and controls. Abnormal EEG tracings were found in 26% of 23 girls with GDPP, two of them with epilepsy. The genotype and allele frequencies of the GABRA1 polymorphisms were not statistically different between unrelated GDPP girls and controls or between GDPP girls with or without EEG abnormalities. CONCLUSIONS: GABRA1 functional mutations or polymorphisms are not associated with the intrinsic mechanism of GDPP in girls with and without EEG abnormalities.
Assuntos
Eletroencefalografia , Gonadotropinas/fisiologia , Mutação , Puberdade Precoce/genética , Receptores de GABA-A/genética , Adolescente , Alelos , Criança , Feminino , Humanos , Subunidades Proteicas , Puberdade Precoce/fisiopatologiaRESUMO
Luteinized intrasplenic ovarian tumors develop in response to high circulating gonadotropins. The relationship between tumor development, gonadotropins and inhibins was studied. Tumor-bearing animals were sacrificed weekly along the first 6 weeks of development. Inhibins were measured by enzyme-linked immunosorbent assay (ELISA), serum gonadotropins, GH and IGF-1 by RIA. Inhibin subunit mRNAs were determined by Northern blot. Tumor histology was examined. Ovarian grafts grew significantly along development. LH increased ten-fold on week 1; a further significant increment was observed on week 3. FSH peaked on weeks 1 and 2 and fell significantly thereafter. Serum inhibins markedly increased on weeks 3-5. Tumor inhibin A content and mRNA levels for alpha and beta A subunits also increased on week 3. Inverse correlations between inhibins and FSH and direct correlations between inhibins and LH were observed. Tumor inhibin A and IGF-1 contents correlated significantly. Increasing levels of luteinization were observed along tumor development. These luteinized tumors develop mainly in response to LH, since growth continues under FSH inhibition. The active inhibin secretion and the positive correlation between inhibins and LH suggests that LH may be the main driving force behind this production, while growth factors produced by the gonads may also participate in their regulation.
Assuntos
Gonadotropinas/fisiologia , Inibinas/fisiologia , Luteinização/fisiologia , Neoplasias Ovarianas/etiologia , Animais , Divisão Celular , Feminino , Hormônio Foliculoestimulante/sangue , Gonadotropinas/sangue , Inibinas/sangue , Inibinas/genética , Fator de Crescimento Insulin-Like I/análise , Hormônio Luteinizante/sangue , Hormônio Luteinizante/fisiologia , Neoplasias Ovarianas/patologia , Subunidades Proteicas/genética , RNA Mensageiro/análise , Ratos , Ratos Sprague-DawleyRESUMO
UNLABELLED: Obese, postmenopausal women have lower FSH levels. To determine whether this is due to higher estrogen exposure, we compared feedback gonadotropin sensitivity and its relation to insulin resistance in four groups of obese and lean, postmenopausal women. Group one was treated with 400 mg troglitazone (TG) daily for two weeks; 150 clomiphene citrate (CC) was added daily for the second week. Group two received 150 mg CC daily for a week. Group three received 1000 mg metformin (MET) daily for two weeks, with 120 mg raloxifene (RAL) added during the second week. Group four received 120 mg RAL for a week. Before and after each period, a serum pool was obtained from samples taken every minute during a 10 ml interval. The women recruited for this study were categorized as obese or lean based on BMI >/= 29 or BMI < 29, respectively. Obese, menopausal women had lower FSH (45.5 IU/l) and LH (16.2 IU/l) values than those of lean (64.1 IU/l and 23.0 IU/l), but the obese menopausal women had higher leptin, DHEAS, glucose, insulin, and HOMA-IR levels. Log [FSH] was associated with BMI (r = -0.53, P < 0.000001) and number of pregnancies (r = -0.37, P = 0.0009). TG treatment did not change HOMA-IR or gonadotropin levels, but DHEAS and androstenedione levels decreased significantly. CC alone or together with TG, diminished FSH (-7.9 and -9.2) and LH (-2.5 and -3.6) concentrations, with a greater reduction in lean women. MET reduced glucose and the HOMA-IR index without affecting gonadotropin or steroid levels. CONCLUSIONS: obese, menopausal women have lower FSH levels due to greater estrogen exposure, by mechanisms unrelated to insulin resistance.
Assuntos
Gonadotropinas/fisiologia , Menopausa/fisiologia , Tiazolidinedionas , Cromanos/administração & dosagem , Cromanos/farmacologia , Clomifeno/administração & dosagem , Clomifeno/farmacologia , Estrogênios/farmacologia , Retroalimentação Fisiológica/fisiologia , Feminino , Hormônio Foliculoestimulante/sangue , Gonadotropinas/sangue , Humanos , Hipoglicemiantes/administração & dosagem , Hipoglicemiantes/farmacologia , Resistência à Insulina , Menopausa/sangue , Metformina/administração & dosagem , Metformina/farmacologia , Pessoa de Meia-Idade , Obesidade/sangue , Gravidez , Cloridrato de Raloxifeno/administração & dosagem , Cloridrato de Raloxifeno/farmacologia , Moduladores Seletivos de Receptor Estrogênico/administração & dosagem , Moduladores Seletivos de Receptor Estrogênico/farmacologia , Tiazóis/administração & dosagem , Tiazóis/farmacologia , TroglitazonaRESUMO
Carbohydrates attached to the protein core of all glycoprotein hormones play an essential role in the function of the molecule, influencing a number of intracellular and extracellular processes. As with other members of the glycoprotein hormone family, pituitary gonadotrophins are not produced as single or unique molecules but rather as arrays of isoforms that differ from each other mainly in the structure of their oligosaccharide attachments. In both experimental animals and in humans, the abundance of the different isoforms varies depending on the endocrine status of the donor present at the time of collection of the tissue or sample. Conditions characterized by an oestrogen-enriched hormonal milieu (eg. the preovulatory phase of the menstrual cycle) promote the formation and secretion of variants with relatively low sialic acid and/or sulphate content, whereas physiological deficiency of this sex steroid (as in the postmenopause) favours the production of highly sialylated, long-lived gonadotrophin variants. When tested individually, less sialylated isoforms exhibit higher receptor-binding and in-vitro biological activity but shorter plasma half-life than their more sialylated counterparts. Both the hormonal regulation and the functional differences among the naturally occurring isoforms strongly suggest that gonadotrophin heterogeneity represents a distinctly different mechanism through which the pituitary gland may regulate the intensity and duration of the gonadotrophic stimulus. Nevertheless, whereas the existence of the alternatively glycosylated variants of gonadotrophins in both the pituitary and in serum is currently without doubt, the physiological role of this phenomenon is still a controversial issue and a matter of debate.
Assuntos
Gonadotropinas/química , Gonadotropinas/fisiologia , Oligossacarídeos/química , Hipófise/metabolismo , Animais , Feminino , Heterogeneidade Genética , Gonadotropinas/sangue , Humanos , Oligossacarídeos/metabolismo , Polimorfismo Genético , Isoformas de ProteínasRESUMO
Este estudo resume o conhecimento atual dos mecanismos envolvidos no consumo folicular no ovário humano. Após o desenvolvimento da gônada e início dos processos de mitose e meiose das oogônias e oócitos, o número de oócitos alcança cerca de 6 a 7 milhöes ao redor da 22ª semana de gravidez. No momento do nascimento o número de oócitos fica reduzido a 1-2 milhöes, refletindo consumo folicular na vida intra-uterina. No início da puberdade o número total de folículos foi reduzido a 400.000. A partir daí, mais de 99,9 por cento dos folículos sofrem degeneraçäo ao longo da vida e apenas 0,1 por cento destes conseguem alcançar um desenvolvimento completo e serem ovulados. Este processo de consumo folicular é um evento complexo. Na vida intra-uterina a mulher perde a maioria dos folículos formados, como resultado de uma taxa de consumo muito rápida. Enquanto gonadotrofinas e certos peptídeos intra-ovarianos atuam como fatores favoráveis à sobrevida dos oócitos nesta fase, os androgênios, um peptídio semelhante ao GnRH e a interleucina-6 säo importantes indutores da atresia. Após o nascimento há diminuiçäo na taxa de consumo folicular e durante o menacme cerca de 1000 folículos säo consumidos a cada mês. Este número é aumentado após os 38 anos de idade, parecendo resultar da aceleraçäo na taxa de crescimento folicular ou de excessiva atresia dos folículos que se encontram em estágios iniciais de desenvolvimento. A apoptose parece ser o mecanismo básico celular de degeneraçäo ou atresia folicular.
Assuntos
Humanos , Animais , Feminino , Apoptose/fisiologia , Atresia Folicular/fisiologia , Hormônios/fisiologia , Ovário/fisiologia , Androgênios/fisiologia , Células Germinativas/fisiologia , Células da Granulosa/citologia , Gonadotropinas/fisiologia , Hormônios/fisiologia , Ovário/citologia , Óvulo/fisiologia , Fatores de TempoRESUMO
Se revisa la frecuencia de amenorrea y esterilidad a la suspención de anticonceptivos hormonales, concluyéndose que ésta es baja. Destaca que la población más susceptible de presentar alteraciones en este sentido es aquella con anteceentes de disfunción hipotálamo-hipofisaria
Assuntos
Amenorreia/fisiopatologia , Anticoncepcionais Orais Hormonais , Anticoncepcionais Orais Hormonais/uso terapêutico , Fertilidade/fisiologia , Galactorreia/etiologia , Gonadotropinas/fisiologia , Infertilidade/fisiopatologia , Menstruação/fisiologia , Ovário/fisiologia , Distúrbios Menstruais/etiologiaRESUMO
The role of lysosomes in the intracellular mechanism of action of several steroid an proteic hormones has been demonstrated. In presence of the specific hormone the target cell induce membranal changes and the lysosomes are moved toward the nucleus; after this the lysosomal enzymes are released in the perinuclear space. For the moment it is not possible to know the biochemical role of this enzymatic activities upon the nucleic acids function and des-repretion process of specific genes, but the inhibition of lysosomes movement utilizing hormone antagonist or dexamethasone inhibits some reproductive process like the implantation of the mammalian egg. We present herein a review related with the mode action of some hormones through the lysosomes in reproductive processes.
Assuntos
Hormônios/fisiologia , Lisossomos/fisiologia , Reprodução , Hormônio Adrenocorticotrópico/fisiologia , Animais , AMP Cíclico/fisiologia , Implantação do Embrião , Estrogênios/fisiologia , Feminino , Gonadotropinas/fisiologia , Humanos , Hidrolases/metabolismo , Técnicas In Vitro , Lisossomos/enzimologia , Lisossomos/genética , Ovário/fisiologia , Hormônios Hipofisários/fisiologia , Gravidez , Prolactina/fisiologia , Ratos , Translocação Genética , Útero/fisiologia , Vasopressinas/fisiologiaRESUMO
La presente revisión tiene por discutir los fenómenos fisiológicos ocurridos en el ciclo ovárico normal de ratas, describiendo el desenvolvimiento de los folículos pre-ovulatorios, las principales hormonas esteroides y gonadotróficas involucradas en este proceso, así como la acción de estas hormonas, a través de su unión a receptores localizados en las células de la granulosa y/o tecales y las modificaciones hormono-dependientes del contenidode tales receptores son también discutidos. La formación del cuerpo lúteo, su posterior regresión y el fenómeno de atresia folicular
Assuntos
Ratos , Ciclo Menstrual/fisiologia , Células da Granulosa , Corpo Lúteo/fisiologia , Atresia Folicular , Gonadotropinas/fisiologia , Folículo Ovariano/fisiologia , Esteroides/fisiologiaRESUMO
El vivir en las grandes alturas, significa someterse a un medio donde predomina una baja presión de oxígeno. Ante tal situación el organismo responde en diversas formas para obtener una adaptación a este medio hipóxico. Estas respuestas pueden ser diferentes de acuerdo a la magnitud de la hipoxia. El estudio de la fisiología de altura, realizado por destacados científicos peruanos se ha constituido en uno de los más importantes campos de investigación en nuestro país en los últimos cincuenta años. En la presente revisión se ha tratado de resumir los trabajos sobre endocrinología en el nativo de la altura, que han realizado diversos investigadores del país y del extranjero, y se ha tratado de explicar en lo posible, las diferencias observadas con respecto a la endocrinología del nativo del nivel del mar. Los resultados demuestran diferencias endocrinas en el nativo de la altura, que están relacionados principalmente en el metabolismo intermedio, y en la reproducción
Assuntos
Humanos , Altitude , Endocrinologia/tendências , Aldosterona/metabolismo , Aldosterona/fisiologia , Clomifeno , Glândulas Suprarrenais/fisiologia , Glândulas Suprarrenais/metabolismo , Teste de Tolerância a Glucose/tendências , Gonadotropinas/metabolismo , Gonadotropinas/fisiologia , Hormônio do Crescimento/metabolismo , Hormônio do Crescimento/fisiologia , Hipotálamo/fisiologia , Hipotálamo/metabolismo , Hidrocortisona/metabolismo , Hidrocortisona/fisiologia , Ovário/metabolismo , Ovário/fisiologia , Hormônios Testiculares/metabolismo , Hormônios Testiculares/fisiologia , Tireotropina/metabolismo , Tireotropina/fisiologiaRESUMO
Fueron comparados dos protocolos de inducción de ovulación, uno con el naálogo LH-RH acetado de leuprolide (27 pacientes) y otro con citrato de clomifeno (18 pacientes), para procedimientos de FIV y TIG. Todas las pacientes habían sido estimuladas anteriormente por diversos inductores y estaban clasificados como un grupo de respuesta pobre. La administración de leuprolide empezó en la fase lútea del ciclo anterior, para eliminar picos prematuros de LH. Con la estimulación por leuprolide se obtuvieron 205 folículos maduros (x +- d.s. = 7.6 +- 4.2, rango 2-20) y 230 ovocitos recuperados (x +- d.s. = 8.5 = +- 4.9, rango 2-22 ). Con la de clomifeno se obtuvieron 76 folículos maduros (x +- d.s. = 4.2 +- 2.3; rango 1-10) y 74 ovocitos recuperados (x +- 4.1 +-2.9; rango 1-11). Estas diferencias fueron estadísticamente significativas. El gran excedente de ovocitos en el grupoleuprolide peritió hacer una reserva de embriones congelados, lo que no fue posible en elg rupo de clomifeno. Se obtuvieron tres embarazos en pacientes del grupo leuprolide y otros tes en un grupo de siete receptores que recibieron embriones u ovocitos donados por pacientes del grupo leuprolide. En ambos casos, un embarazo fue por FIV y dos por TIG. No hubo embarazos en el grupo de pacientes tratadas con colomifeno. Este estudio confirma la ventaja del uso del análogo LH-RH acetato de leuprolide, por la obtención de mayor cantidad de folículos maduros, de ovocitos y de embriones, y por la mayor tasa de embarazos, además de la mayor facilidad para el equipo médico y la comodidad para las pacientes.