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      CONCEPTOS ACTUALES SOBRE MECANISMOS REGULADORES DE LA PUBERTAD Translated title: Current concepts regarding mechanisms regulating puberty

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          Abstract

          El inicio de la pubertad depende de la activación del eje hipotálamo-hipofisiario-gonadal. Existe una red glial y neuronal que interactúa por medio de moléculas de adhesión, factores de crecimiento, aminoácidos, péptidos y derivados lipídicos, que permiten integrar en el hipotálamo la información del estado metabólico del individuo con la que proviene del medio ambiente determinando el comienzo y mantenimiento de la etapa reproductiva. En los últimos años se ha ampliado la comprensión de los factores que intervienen en la pubertad, aunque no se han dilucido todos los mecanismos participantes. Este artículo revisa algunos de los procesos celulares y moleculares más importantes en la regulación de la secreción pulsátil de GnRH, con mayor énfasis en los conocimientos más recientes.

          Translated abstract

          The onset of puberty depends on activating the hypothalamic-pituitary-gonadal axis. A glial and neuronal network interacts by means of adhesion molecules, growth factors, amino acids, peptides and lipid derivates, leading to information about an individual's metabolic state becoming integrated with that from the environment in the hypothalamus and thereby determining the start of the reproductive stage and its maintenance. Understanding about the factors intervening in puberty has become greater during the last few years, even though all the participating mechanisms have not yet been elucidated. This article reviews some of the most important cellular and molecular processes in regulating pulsatile gonadotropin-releasing hormone (GnRH) secretion, placing greater emphasis on the most recent knowledge.

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          Most cited references69

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          Differential regulation of KiSS-1 mRNA expression by sex steroids in the brain of the male mouse.

          Kisspeptins are products of the Kiss1 gene, which bind to GPR54, a G protein-coupled receptor. Kisspeptins and GPR54 have been implicated in the neuroendocrine regulation of GnRH secretion. To test the hypothesis that testosterone regulates Kiss1 gene expression, we compared the expression of KiSS-1 mRNA among groups of intact, castrated, and castrated/testosterone (T)-treated male mice. In the arcuate nucleus (Arc), castration resulted in a significant increase in KiSS-1 mRNA, which was completely reversed with T replacement, whereas in the anteroventral periventricular nucleus, the results were the opposite, i.e. castration decreased and T increased KiSS-1 mRNA expression. In the Arc, the effects of T on KiSS-1 mRNA were completely mimicked by estrogen but only partially mimicked by dihydrotestosterone, a nonaromatizable androgen, suggesting that both estrogen receptor (ER) and androgen receptor (AR) play a role in T-mediated regulation of KiSS-1. Studies of the effects of T on KiSS-1 expression in mice with either a deletion of the ERalpha or a hypomorphic allele to the AR revealed that the effects of T are mediated by both ERalpha and AR pathways, which was confirmed by the presence of either ERalpha or AR coexpression in most KiSS-1 neurons in the Arc. These observations suggest that KiSS-1 neurons in the Arc, whose transcriptional activity is inhibited by T, are targets for the negative feedback regulation of GnRH secretion, whereas KiSS-1 neurons in the anteroventral periventricular nucleus, whose activity is stimulated by T, may mediate other T-dependent processes.
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            Definitive evidence for the existence of morphological plasticity in the external zone of the median eminence during the rat estrous cycle: implication of neuro-glio-endothelial interactions in gonadotropin-releasing hormone release

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              The roles of kisspeptins and G protein-coupled receptor-54 in pubertal development.

              This review summarizes the experimental data demonstrating the fundamental role of kisspeptins and their G protein-coupled receptor GPR54 in the control of reproduction, with special emphasis on their function at puberty. Kisspeptins, products of the KiSS-1 gene, were originally identified as metastasis suppressor peptides with the ability to bind G protein-coupled receptor GPR54. In late 2003, loss-of-function mutations of the GPR54 gene were found in patients suffering from hypogonadotropic hypogonadism. This finding kicked off the analysis of the role of the KiSS-1/GPR54 system in the control of reproduction. Kisspeptins are very potent elicitors of gonadotropin secretion, primarily through stimulation of gonadotropin-releasing hormone release. Enhanced expression of KiSS-1 and GPR54 genes, as well as increased GPR54 signaling, are detected at the hypothalamus during pubertal development, and activation of GPR54 by administration of kisspeptin is sufficient to induce precocious activation of the gonadotropic axis in immature rodents and monkeys. Hypothalamic KiSS-1 also functions as an essential integrator for peripheral inputs, including gonadal steroids and nutritional signals, controlling gonadotropin-releasing hormone and gonadotropin secretion. Kisspeptins and their putative receptor, GPR54, have recently emerged as indispensable factors for pubertal development, with a key role as gatekeepers of gonadotropin-releasing hormone release neurons and, hence, of reproductive function.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Journal
                rfmun
                Revista de la Facultad de Medicina
                rev.fac.med.
                Universidad Naciona de colombia (Bogotá )
                0120-0011
                March 2012
                : 60
                : 1
                : 50-59
                Affiliations
                [1 ] Universidad Nacional de Colombia
                [2 ] Universidad Nacional de Colombia
                Article
                S0120-00112012000100006
                fea8a1a4-bf95-403c-8d50-ee52f2771cd4

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

                History
                Product

                SciELO Colombia

                Self URI (journal page): http://www.scielo.org.co/scielo.php?script=sci_serial&pid=0120-0011&lng=en
                Categories
                MEDICINE, GENERAL & INTERNAL

                Internal medicine
                puberty,metablic phenomena,hypothalamus,recptors,LHRH (MeSH),pubertad,fenómenos metabólicos,hipotálamo,receptores),LHRH (GnRH) (DeCS

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