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Endocrine Functions of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Kisspeptins are a group of peptides ranging from 10 to 54 amino acids that are derived from a single precursor. They bind to and activate the G protein-coupled receptor Kiss1R with similar efficacy [68]. The hypothalamic kisspeptin neurons play a key role in regulating the activity of GnRH neurons [69]. In both rodents and sheep, the kisspeptin neurons in the preoptic area are sexually dimorphic, being more numerous in females than males. There are two major groups of kisspeptin cell bodies: a large number in the arcuate nucleus, and a smaller number in the periventricular area of the third ventricle of rodents and the preoptic area of non-rodents [70].
Genetic Causes of Male Infertility
Published in Botros Rizk, Ashok Agarwal, Edmund S. Sabanegh, Male Infertility in Reproductive Medicine, 2019
Amr Abdel Raheem, Mohamed Wael Ragab, Tarek M. A. Aly
Impairment of gonadotropin secretion may result from decreased gonadotropin-releasing hormone (GnRH) production, which leads to quantitative decrease in spermatogenesis. Hypogonadotropic hypogonadism can occur due to congenital or acquired causes. Monogenetic mutations account for around 50% of cases and contribute to CHH via several modes of inheritance, including monogenic autosomal or X-linked (dominant or recessive forms) and oligogenic [51]. Genetic mutations involving FGFR1, FGF8, and SOX10 disrupt embryonic development of GnRH neurons, whereas ANOS1 (formally KAL1), PROK2, PROK2R, and CHD7 impair migration of GnRH neurons from the olfactory placode to the hypothalamus. Other mutations that are associated with GnRH neuron dysregulation involve TAC3, TACR3, KISS1, KISS1R, and OTUD4 genes. Additionally, mutations of GnRH1 gene and its receptor (GnRHR) manifest with CHH [52]. In addition to hypogonadism, certain phenotypic features may be associated with some of the genetic causes of CHH, including anosmia (Kallmann syndrome), cryptorchidism, micro-penis, cleft lip or palate, and renal agenesis [51].
Intrinsic and Extrinsic Factors That Influence Epigenetics
Published in Cristina Camprubí, Joan Blanco, Epigenetics and Assisted Reproduction, 2018
Ivan Nalvarte, Joëlle Rüegg, Carlos Guerrero-Bosagna
The initiation of mammalian puberty is orchestrated by a myriad of complex interactions involving different cell types and organs that activate large and interconnected gene networks. Although the molecular mechanisms are still largely obscure, from a neuronal perspective it is known that puberty is triggered by trans-synaptic (24,25) and glial (26) interactions with hypothalamic neurons that release GnRH. Kisseptins are neuropeptides that have a major role in GnRH release. Kisspeptins are transcribed from the KISS1 gene and bind to the kisseptin receptor (GPR54/KISS1R) on GnRH neurons of the hypothalamus (24,27,28). GnRH, in turn, triggers the release of LH and FSH from the anterior pituitary, leading to downstream effects in hormonal levels related to pubertal progression, development of secondary sexual characteristics, and ovulation in females. De-methylation of a regulatory region of the GNRH gene seems to be one of the mechanisms of regulation of GnRH release during puberty (29).
The Kisspeptin and Kisspeptin receptor in follicular microenvironment: is that really necessary for oocyte maturation and fertilisation?
Published in Journal of Obstetrics and Gynaecology, 2022
Goktan Kuspinar, Cihan Cakır, Isıl Kasapoglu, Seda Saribal, Barbaros Oral, Ferah Budak, Gurkan Uncu, Berrin Avcı
Kisspeptin is an essential regulator of reproductive function (de Roux et al. 2003; Seminara et al. 2003) and plays a key role in the modulation of GnRH secretion and gonadotropin release (Roa et al. 2006). In humans, kisspeptin (KISS1) is encoded by the KISS1 gene, and its effects are mediated by the KISS1 receptor (KISS1R), which is encoded by the KISS1R gene (Seminara et al. 2003). The mutations of KISS1R gene in humans and mice with hypogonadotropic hypogonadism and the observation of damaged pubertal development in these cases showed that the role of the KISS1 and KISS1R in the reproductive system (de Roux et al. 2003; Seminara et al. 2003). In ART cycles, inducing luteinizing hormone (LH) surge effectively with the administration of kisspeptin has been reported to successful final human oocyte maturation and live birth (Abbara et al. 2014). Current animal studies have shown that supplementation of KISS1 to in vitro maturation culture medium is enhanced oocyte maturation (Saadeldin et al. 2012). Moreover, follicular development is arrested at the antral stage in KISS1 or KISS1R null mice, suggesting a role in follicular development regulation (Calder et al. 2014). Although studies were evaluated especially peripheric or local kisspeptin levels in both humans and animals, the specific role of KISS1 and KISS1R on oocyte maturation and fertilisation status in humans has not been elucidated yet.
Association analysis of KISS1 polymorphisms and haplotypes with polycystic ovary syndrome
Published in British Journal of Biomedical Science, 2021
M Farsimadan, F Moammadzadeh Ghosi, S Takamoli, H Vaziri
KISS1 and KISS1R are the first genes involved in gonadotropin-dependent precocious puberty (GDPP) phenotypes in humans. Patients with KISS1 mutations exhibit typical features of idiopathic GDPP and show an adequate response to conventional GDPP treatment with GnRH agonists [18,19]. Different investigations have studied KISS1 mutations in disorders of puberty. In a very recent study on a large group of girls, Li et al. evaluated the association of KISS1 polymorphism with the risk of central precocious puberty (CPP) and their results suggested that the mutation in rs5780218 increases the risk of CPP [20]. Similarly, the results of another study among Chinese girls diagnosed with CPP uncovered several potentially polymorphisms in KISS1 and reported the frequency of these SNPs to be significantly higher among patients compared with controls [21]. Likewise, Silveira et al. demonstrated two different missense mutations in KISS1 be associated with a higher risk of isolated hypogonadotropic hypogonadism (IHH) and CPP [11]. However, some studies failed to show any relationship between the KISS1 polymorphisms and increased risks of CPP [22,23] and IHH [24].
Insulin resistance and potential modulators of ovarian reserve in young reproductive-aged women with obesity and type 1 diabetes
Published in Gynecological Endocrinology, 2021
Valeria Calcaterra, Rossella E. Nappi, Gloria Pelizzo, Annalisa De Silvestri, Riccardo Albertini, Mara De Amici, Elisavietta Tenuta, Federica Vinci, Chiara Mameli, Gianvincenzo Zuccotti
The interaction between some adipokines, such as adiponectin, and kisspeptin, an essential gatekeeper of puberty, has been described in the context of ovarian physiology. Adiponectin and its receptors are expressed in hypothalamic-pituitary-gonadal axis and their activation regulates Kiss, GnRH and gonadotropin expression [16]. In particular, adiponectin can reduce GnRH secretion and can inhibit Kiss1 gene transcription [44–46]; as a result, the promoter activity and transcription levels of KISS1 gene are repressed [45]. KISS1 gene encodes the neuropeptide kisspeptin, which is an active ligand of GPR54 (KISS1R) in humans [47]. The KISS1/GPR54 system plays a crucial role in the neuroendocrine control of the gonadotrophin axis: kisspeptin is secreted by hypothalamus and stimulates the release of GnRH [47]. The neuropeptide kisspeptin is also expressed in different ovarian tissues, suggesting a role for kisspeptin in ovarian function [47,48]. The significant temporal and spatial specificity of such expression suggests that the kisspeptin/KISS1R system performs multiple functions from infancy to transitional age at different physiological stages in the ovary, including follicular development, oocyte maturation, ovulation and ovarian steroidogenesis [48].