scholarly journals Androgen-dependent sexual dimorphism in pituitary tryptophan hydroxylase expression: relevance to sex differences in pituitary hormones

2020 ◽  
Vol 287 (1928) ◽  
pp. 20200713
Author(s):  
Yukika Kawabata-Sakata ◽  
Yuji Nishiike ◽  
Thomas Fleming ◽  
Yukiko Kikuchi ◽  
Kataaki Okubo

Serotonin is a biogenic monoamine conserved across phyla that is implicated in diverse physiological and behavioural functions. On examining the expression of the rate-limiting enzymes in serotonin synthesis, tryptophan hydroxylases (TPHs), in the teleost medaka ( Oryzias latipes ), we found that males have much higher levels of tph1 expression as compared with females. This robust sexual dimorphism was found to probably result from the direct stimulation of tph1 transcription by androgen/androgen receptor binding to canonical bipartite androgen-responsive elements in its proximal promoter region. Our results further revealed that tph1 expression occurs exclusively in pro-opiomelanocortin ( pomc )-expressing cells and that the resulting serotonin and its derivative melatonin inhibit the expression of the pituitary hormone genes, fshb , sl and tshb . This suggests that serotonin and/or melatonin synthesized in pomc -expressing cells act in a paracrine manner to suppress pituitary hormone levels. Consistent with these findings and the male-biased expression of tph1 , the expression levels of fshb , sl and tshb were all higher in females than in males. Taken together, the male bias in tph1 expression and consequent serotonin/melatonin production presumably contribute to sex differences in the expression of pituitary hormones and ultimately in the physiological functions mediated by them.

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Junpei Yamashita ◽  
Yuji Nishiike ◽  
Thomas Fleming ◽  
Daichi Kayo ◽  
Kataaki Okubo

AbstractThe preoptic area (POA) is one of the most evolutionarily conserved regions of the vertebrate brain and contains subsets of neuropeptide-expressing neurons. Here we found in the teleost medaka that two neuropeptides belonging to the secretin family, pituitary adenylate cyclase-activating polypeptide (Pacap) and vasoactive intestinal peptide (Vip), exhibit opposite patterns of sexually dimorphic expression in the same population of POA neurons that project to the anterior pituitary: Pacap is male-biased, whereas Vip is female-biased. Estrogen secreted by the ovary in adulthood was found to attenuate Pacap expression and, conversely, stimulate Vip expression in the female POA, thereby establishing and maintaining their opposite sexual dimorphism. Pituitary organ culture experiments demonstrated that both Pacap and Vip can markedly alter the expression of various anterior pituitary hormones. Collectively, these findings show that males and females use alternative preoptic neuropeptides to regulate anterior pituitary hormones as a result of their different estrogen milieu.


2021 ◽  
Vol 22 (9) ◽  
pp. 4620
Author(s):  
Holly J. Woodward ◽  
Dongxing Zhu ◽  
Patrick W. F. Hadoke ◽  
Victoria E. MacRae

Sex differences in cardiovascular disease (CVD), including aortic stenosis, atherosclerosis and cardiovascular calcification, are well documented. High levels of testosterone, the primary male sex hormone, are associated with increased risk of cardiovascular calcification, whilst estrogen, the primary female sex hormone, is considered cardioprotective. Current understanding of sexual dimorphism in cardiovascular calcification is still very limited. This review assesses the evidence that the actions of sex hormones influence the development of cardiovascular calcification. We address the current question of whether sex hormones could play a role in the sexual dimorphism seen in cardiovascular calcification, by discussing potential mechanisms of actions of sex hormones and evidence in pre-clinical research. More advanced investigations and understanding of sex hormones in calcification could provide a better translational outcome for those suffering with cardiovascular calcification.


2021 ◽  
Vol 22 (15) ◽  
pp. 8111
Author(s):  
Kuang-Hsu Lien ◽  
Chao-Hui Yang

The triad of noise-generated, drug-induced, and age-related hearing loss is the major cause of acquired sensorineural hearing loss (ASNHL) in modern society. Although these three forms of hearing loss display similar underlying mechanisms, detailed studies have revealed the presence of sex differences in the auditory system both in human and animal models of ASNHL. However, the sexual dimorphism of hearing varies among noise-induced hearing loss (NIHL), ototoxicity, and age-related hearing loss (ARHL). Importantly, estrogen may play an essential role in modulating the pathophysiological mechanisms in the cochlea and several reports have shown that the effects of hormone replacement therapy on hearing loss are complex. This review will summarize the clinical features of sex differences in ASNHL, compare the animal investigations of cochlear sexual dimorphism in response to the three insults, and address how estrogen affects the auditory organ at molecular levels.


BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Basabi Bagchi ◽  
Quentin Corbel ◽  
Imroze Khan ◽  
Ellen Payne ◽  
Devshuvam Banerji ◽  
...  

Abstract Background Sexual dimorphism in immunity is believed to reflect sex differences in reproductive strategies and trade-offs between competing life history demands. Sexual selection can have major effects on mating rates and sex-specific costs of mating and may thereby influence sex differences in immunity as well as associated host–pathogen dynamics. Yet, experimental evidence linking the mating system to evolved sexual dimorphism in immunity are scarce and the direct effects of mating rate on immunity are not well established. Here, we use transcriptomic analyses, experimental evolution and phylogenetic comparative methods to study the association between the mating system and sexual dimorphism in immunity in seed beetles, where mating causes internal injuries in females. Results We demonstrate that female phenoloxidase (PO) activity, involved in wound healing and defence against parasitic infections, is elevated relative to males. This difference is accompanied by concomitant sex differences in the expression of genes in the prophenoloxidase activating cascade. We document substantial phenotypic plasticity in female PO activity in response to mating and show that experimental evolution under enforced monogamy (resulting in low remating rates and reduced sexual conflict relative to natural polygamy) rapidly decreases female (but not male) PO activity. Moreover, monogamous females had evolved increased tolerance to bacterial infection unrelated to mating, implying that female responses to costly mating may trade off with other aspects of immune defence, an hypothesis which broadly accords with the documented sex differences in gene expression. Finally, female (but not male) PO activity shows correlated evolution with the perceived harmfulness of male genitalia across 12 species of seed beetles, suggesting that sexual conflict has a significant influence on sexual dimorphisms in immunity in this group of insects. Conclusions Our study provides insights into the links between sexual conflict and sexual dimorphism in immunity and suggests that selection pressures moulded by mating interactions can lead to a sex-specific mosaic of immune responses with important implications for host–pathogen dynamics in sexually reproducing organisms.


2012 ◽  
Vol 60 (2) ◽  
pp. 101 ◽  
Author(s):  
Thomas E. White ◽  
Joseph Macedonia ◽  
Debra Birch ◽  
Judith Dawes ◽  
Darrell J. Kemp

Structurally generated colours are at least as commonplace and varied components of animal signals as pigment colours, yet we know far less about the former, both in terms of the patterns and phenotypic variation and of their underlying correlates and causes. Many butterflies exhibit bright and iridescent colour signals that arise from a characteristic ‘ridge-lamellar’ scale surface nanoarchitecture. Although there are multiple axes of functional variation in these traits, few have been investigated. Here we present evidence that sexual dimorphism in the expression of a sexually homologous ridge-lamellar trait (iridescent ultraviolet) is mediated by sex differences in the density of lamellar-bearing scale ridges. This trait – ridge density – has also been causally related to iridescent signal variation in other coliadines (e.g. C. eurytheme), which suggests that it may offer a common basis to both intra- and intersexual differences in ultraviolet wing reflectance among these butterflies.


1987 ◽  
Vol 113 (2) ◽  
pp. 183-192 ◽  
Author(s):  
C. H. G. Irvine ◽  
S. L. Alexander

ABSTRACT We have described a novel technique for collecting pituitary venous effluent in the horse by placing a cannula in the intercavernous sinus close to the outlet of the pituitary veins using a venous pathway unique to equids. Cannula placement and blood collection are carried out painlessly in fully conscious, ambulatory, unstressed animals. There is no interference to hypothalamic, pituitary or target organ function. The blood collected contains readily measurable concentrations of gonadotrophin-releasing hormone, and LH concentrations which can be up to 40 times those in concurrent peripheral blood samples. Four millilitre blood samples, a quantity which permits simultaneous measurement of many hypothalamic and pituitary hormones, can be collected at 2-min intervals for several days. Intercavernous sinus blood flow can be calculated allowing secretion rates of hypothalamic and pituitary hormones to be determined for any time-period. This model is uniquely useful for investigating the normal functional characteristics of several neuroendocrine and endocrine systems. J. Endocr. (1987) 113, 183–192


1993 ◽  
Vol 129 (6) ◽  
pp. 489-496 ◽  
Author(s):  
Andreas Kjær

Secretion of the anterior pituitary hormones adrenocorticotropin (ACTH), β-endorphin and prolactin (PRL) is complex and involves a variety of factors. This review focuses on the involvement of arginine-vasopressin (AVP) in neuroendocrine regulation of these anterior pituitary hormones with special reference to receptor involvement, mode of action and origin of AVP. Arginine-vasopressin may act via at least two types of receptors: V1− and V2−receptors, where the pituitary V1−receptor is designated V1b. The mode of action of AVP may be mediating, i.e. anterior pituitary hormone secretion is transmitted via release of AVP, or the mode of action may be permissive, i.e. the presence of AVP at a low and constant level is required for anterior pituitary hormones to be stimulated. Under in vivo conditions, the AVP-induced release of ACTH and β-endorphin is mainly mediated via activation of hypothalamic V1− receptors, which subsequently leads to the release of corticotropin-releasing hormone. Under in vitro conditions, the AVP-stimulated release of ACTH and β-endorphin is mediated via pituitary V1b− receptors. The mode of action of AVP in the ACTH and β-endorphin response to stress and to histamine, which is involved in stress-induced secretion of anterior pituitary hormones, is mediating (utilizing V1− receptors) as well as permissive (utilizing mainly V1− but also V2−receptors). The AVP-induced release of PRL under in vivo conditions is conveyed mainly via activation of V1−receptors but V2−receptors and probably additional receptor(s) may also play a role. In stress- and histamine induced PRL secretion the role of AVP is both mediating (utilizing V1 −receptors) and permissive (utilizing both V1− and V2− receptors). Arginine-vasopressin may be a candidate for the PRL-releasing factor recently identified in the posterior pituitary gland. Arginine-vasopressin of both magno- and parvocellular origin may be involved in the regulation of anterior pituitary hormone secretion and may reach the corticotrophs and the lactotrophs via three main routes: the peripheral circulation, the long pituitary portal vessels or the short pituitary portal vessels.


2021 ◽  
Vol 135 (24) ◽  
pp. 2691-2708
Author(s):  
Simon T. Bond ◽  
Anna C. Calkin ◽  
Brian G. Drew

Abstract The escalating prevalence of individuals becoming overweight and obese is a rapidly rising global health problem, placing an enormous burden on health and economic systems worldwide. Whilst obesity has well described lifestyle drivers, there is also a significant and poorly understood component that is regulated by genetics. Furthermore, there is clear evidence for sexual dimorphism in obesity, where overall risk, degree, subtype and potential complications arising from obesity all differ between males and females. The molecular mechanisms that dictate these sex differences remain mostly uncharacterised. Many studies have demonstrated that this dimorphism is unable to be solely explained by changes in hormones and their nuclear receptors alone, and instead manifests from coordinated and highly regulated gene networks, both during development and throughout life. As we acquire more knowledge in this area from approaches such as large-scale genomic association studies, the more we appreciate the true complexity and heterogeneity of obesity. Nevertheless, over the past two decades, researchers have made enormous progress in this field, and some consistent and robust mechanisms continue to be established. In this review, we will discuss some of the proposed mechanisms underlying sexual dimorphism in obesity, and discuss some of the key regulators that influence this phenomenon.


2014 ◽  
Vol 281 (1790) ◽  
pp. 20140333 ◽  
Author(s):  
Crystal M. Vincent ◽  
Darryl T. Gwynne

Sex differences in immunity are often observed, with males generally having a weaker immune system than females. However, recent data in a sex-role-reversed species in which females compete to mate with males suggest that sexually competitive females have a weaker immune response. These findings support the hypothesis that sexual dimorphism in immunity has evolved in response to sex-specific fitness returns of investment in traits such as parental investment and longevity, but the scarcity of data in sex-reversed species prevents us from drawing general conclusions. Using an insect species in which males make a large but variable parental investment in their offspring, we use two indicators of immunocompetence to test the hypothesis that sex-biased immunity is determined by differences in parental investment. We found that when the value of paternal investment was experimentally increased, male immune investment became relatively greater than that of females. Thus, in this system, in which the direction of sexual competition is plastic, the direction of sex-biased immunity is also plastic and appears to track relative parental investment.


2014 ◽  
Vol 15 (3) ◽  
pp. 115-120
Author(s):  
Verica Milošević ◽  
Vladimir Ajdžanović

Abstract Female ageing represents the biological process of structural and functional changes in endocrine cells and tissues, as well as in pituitary hormone-producing cells. In addition to the hypothalamic releasing hormones, estradiol plays a significant role in the regulation of the synthesis/secretion of pituitary hormones and is still used therapeutically for menopausal symptoms. The effects of ageing or ovariectomy and synthetic estradiol application under these circumstances were evaluated in pituitary hormone-producing cells of female rats (animal models of menopause); i.e., the following cells were observed: gonadotropes (FSH and LH), thyrotropes (TSH), somatotropes (GH), mammotropes (PRL) and corticotropes (ACTH). The cells were immunostained and histologically analysed. The ELISA method was used for hormonal analyses. Ageing was found to cause diverse, commonly reductive changes regarding the volume, number and secretion of menopausal rat pituitary hormone- producing cells, except for PRL cells that exhibit significantly increased numbers and intensified secretion. After the treatment of middle-aged female rats wiThestradiol, the absolute and relative pituitary weights significantly increased in comparison with the control females. Histological parameters such as the cell and volume density of PRL and ACThcells were significantly increased compared with the control values. The mentioned parameters of FSH, LH, GH, and occasionally TSH cells after estradiol treatment significantly decreased in comparison with the controls. The corresponding hormone levels followed the changes in the histological parameters. These data indicate that the application of estradiol to menopausal females may specifically, in two directions, modify the histological characteristics and secretory activities of different pituitary-hormone producing cells..


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