Precocious puberty [locus GNRH,LHRH 8p21-p11.2 (152760), IHH 19p13.3 (146110)]§§, is usually defined as onset of menarche in the female to generate the luteinizing hormone (LH) surge component of LHRH responsible for ovulation, rarer in females is familial precocious puberty with primary failure of GNRH in girls (X-linked recessive inheritance) is idiopathic KISS1R metastin receptor hoT7T175 mild increase in estrogen secretion agonist treatment from premature activation of the hypothalamic-pituitary-gonadal axis GNRHR1 located in [19p13.3, 9q34.3, 3p21.1] the metabolic pathways of the arcuate nucleus of the hypothalamus where the GNRH pulse generator is encoded by 1 DNA strand, in men that have severe deficiency of GNRH, in the hypothalamic-pituitary-gonadal axis that controls human reproduction signaling is not required for male or female copulatory behavior, provided there is appropriate adulthood hormone replacement, the treatment is not likely to be a substantial modulator of pubertal timing inhibitition in the general population.
Loss of function of GPR54 [KiSS-1R] is a cause of IHH, mainly through regulation of GnRH secretion at the hypothalamus. Yet the actual role of the KiSS-1/GPR54 system is-derived peptide metastin supressor of the KiSS1R/GPR54 receptor mutations in KISS1 the system is critical to normal reproductive development, metastasis suppression is not mediated through this receptor though kisspeptins, or mimetics could be used to maintain tumor dormancy. The hypothalamic KiSS-1/GPR54 system has been proven as an essential gatekeeper of GnRH neurons, however interactions (autocrine, paracrine, and/or endocrine) could also impact tumour behaviour in a negative manner.
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