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      Analysis of testosterone pulsatility in women with ovulatory menstrual cycles Translated title: Análise da pulsatilidade da testosterona em mulheres com ciclos menstruais ovulatórios

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          Abstract

          OBJECTIVE: To evaluate the pattern of the pulsatile secretion of testosterone in normal menstrual cycle. METHODS: Eight healthy women with ovulatory menstrual cycles were enrolled. Blood samples were collected at ten-minute intervals for six hours, starting between 7 and 8 am, after a ten-hour fasting, in three phases: mid-follicular (Day 7), late follicular (Day 12) and mid-luteal phase (Day 21). Samples were assayed for testosterone, LH and the baseline also for SHBG. RESULTS: Testosterone pulse frequency, mean amplitude pulse, percentage of increment in pulse amplitude, mean duration of pulses and pulse interval were similar in the three phases. LH pulsatility was statistically different among the three phases (p < 0.001) representing normal ovulatory cycles. CONCLUSIONS: These data increase the knowledge about the testosterone secretion profile in the human menstrual cycle and can be used as a contribution to clinical investigation in both hyperandrogenism and androgen insufficiency syndrome.

          Translated abstract

          OBJETIVO: Avaliar o padrão pulsátil da secreção da testosterona em mulheres normais. MÉTODOS: Oito mulheres saudáveis com ciclos ovulatórios foram selecionadas. Amostras sanguíneas foram coletadas a cada dez minutos durante seis horas, começando entre 7 e 8 h da manhã, após dez horas de jejum, nas três fases do ciclo menstrual: folicular média (Dia 7), folicular tardia (Dia 12) e lútea (Dia 21). Foram mensurados: testosterona, LH e, no basal, também SHBG. RESULTADOS: A frequência dos pulsos de testosterona, média da amplitude do pulso, porcentagem do incremento da amplitude, duração e intervalos dos pulsos foram similares nas três fases (p > 0,05). A pulsatilidade do LH foi estatisticamente diferente entre as três fases (p < 0,001), caracterizando padrão característico do ciclo ovulatório normal. CONCLUSÕES: Esses dados aumentam o conhecimento sobre o padrão de secreção da testosterona no ciclo menstrual humano e representam uma contribuição para a investigação clínica, tanto no hiperandrogenismo como na síndrome de insuficiência androgênica.

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          Most cited references39

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          Polycystic Ovary Syndrome

          New England Journal of Medicine, 352(12), 1223-1236
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            Testosterone and cognitive function: current clinical evidence of a relationship.

            Testosterone levels decline as men age, as does cognitive function. Whether there is more than a temporal relationship between testosterone and cognitive function is unclear. Chemical castration studies in men with prostate cancer suggest that low serum testosterone may be associated with cognitive dysfunction. Low testosterone levels have also been observed in patients with Alzheimer's disease (AD) and mild cognitive impairment (MCI). This paper reviews the current clinical evidence of the relationship between serum testosterone levels and cognitive function in older men. A systematic literature search was conducted using PubMed and EMBASE to identify clinical studies and relevant reviews that evaluated cognitive function and endogenous testosterone levels or the effects of testosterone substitution in older men. Low levels of endogenous testosterone in healthy older men may be associated with poor performance on at least some cognitive tests. The results of randomized, placebo-controlled studies have been mixed, but generally indicate that testosterone substitution may have moderate positive effects on selective cognitive domains (e.g. spatial ability) in older men with and without hypogonadism. Similar results have been found in studies in patients with existing AD or MCI. Low endogenous levels of testosterone may be related to reduced cognitive ability, and testosterone substitution may improve some aspects of cognitive ability. Measurement of serum testosterone should be considered in older men with cognitive dysfunction. For men with both cognitive impairment and low testosterone, testosterone substitution may be considered. Large, long-term studies evaluating the effects of testosterone substitution on cognitive function in older men are warranted.
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              The neuroendocrinology of human puberty revisited.

              The fundamental aspects of the hypothalamic luteinizing hormone-releasing hormone (LHRH)(1) [1]pulse generator-pituitary gonadotrophin-gonadal apparatus in mammals have striking commonalities. There are, however, critical, substantive differences in the neuroendocrinology of puberty among species. The onset of puberty in the human is marked by an increase in the amplitude of LH pulses, an indirect indicator of the increase in amplitude of LHRH pulses. The hypothalamic LHRH-pituitary gonadotrophin complex is functional by at least 0.3 gestation in the human foetus; the sex difference in the fetal and neonatal pattern of LH and FSH secretion is an apparent consequence of imprinting of the fetal hypothalamus-pituitary-gonadotropin apparatus by fetal testosterone. Until about 6 months of age in boys and 12-24 months in girls, the testes and ovaries respond to the increased LH in boys and follicle-stimulating hormone (FSH) in girls by secreting testosterone and oestradiol, respectively, reaching levels that are not again achieved before the onset of puberty. Striking features of the ontogeny of the human hypothalamic pulse generator are: (1) its development and function in the foetus; (2) the continued function of the hypothalamic LHRH pulse generator-pituitary gonadotrophin-gonadal axis in infancy; (3) the gradual damping of hypothalamic LHRH oscillator activity during late infancy; (4) its quiescence during childhood - the so-called juvenile pause; (5) during late childhood the gradual disinhibition and reactivation of the LHRH pulse generator, mainly at night; (6) the increasing amplitude of the LHRH pulses, which are reflected in the progressively increased and changing pattern of circulating LH pulses, with the approach of and during puberty. The intrinsic central nervous system (CNS) mechanisms responsible for the inhibition of the LHRH pulse generator during childhood (the juvenile phase) involve the major role of an inhibitory neuronal system - the CNS inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and GABAergic neurons, as revealed by studies in the rhesus monkey by Terasawa and her associates. With the onset of puberty, the disinhibition and reactivation of the LHRH pulse generator is associated with a fall in GABAergic neurotransmission and a concomitant increase in the input of excitatory amino acid neurotransmitters (including glutamate) and possibly astroglial-derived growth factors. Despite remarkable progress over the past three decades, large gaps remain in our understanding of the neurobiological, genetic and environmental mechanisms involved in the control of the onset of puberty. The role of leptin in the control of the onset of puberty is reviewed. Severe leptin deficiency is associated with hypogonadotrophic hypogonadism; it appears that a critical level of leptin and a leptin signal is required to achieve puberty. The weight of evidence supports the hypothesis that leptin acts as one of several permissive factors and not a trigger in the onset of human puberty. The application of these advances provides a framework for the described classification of sexual precocity and delayed puberty.1 GnRH is synonymous with LHRH. Copyright 2002 S. Karger AG, Basel
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                abem
                Arquivos Brasileiros de Endocrinologia & Metabologia
                Arq Bras Endocrinol Metab
                Sociedade Brasileira de Endocrinologia e Metabologia (São Paulo )
                1677-9487
                November 2009
                : 53
                : 8
                : 1040-1046
                Affiliations
                [1 ] Universidade Federal do Rio Grande do Norte Brazil
                [2 ] Universidade Federal do Rio Grande do Norte Brazil
                [3 ] Universidade de São Paulo Brasil
                [4 ] Universidade Federal do Rio Grande do Sul Brasil
                Article
                S0004-27302009000800020
                10.1590/S0004-27302009000800020
                20126859
                8d9a653b-256c-4310-8bdd-6f3f0cccbc43

                http://creativecommons.org/licenses/by/4.0/

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                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=0004-2730&lng=en
                Categories
                ENDOCRINOLOGY & METABOLISM

                Endocrinology & Diabetes
                Testosterone,pulse,menstrual cycle,Testosterona,pulsatilidade,ciclo menstrual
                Endocrinology & Diabetes
                Testosterone, pulse, menstrual cycle, Testosterona, pulsatilidade, ciclo menstrual

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