scholarly journals Hormonal and neuroendocrine control of reproductive function in teleost fish.

Bionatura ◽  
2021 ◽  
Vol 3 (3) ◽  
pp. 2122-2133
Author(s):  
Adrian Rodríguez Gabilondo ◽  
Liz Hernández Pérez ◽  
Rebeca Martínez Rodríguez
Keyword(s):  
Follicle Stimulating Hormone ◽  
Reproductive Function ◽  
Gonadotropin Releasing Hormone ◽  
Reproductive Physiology ◽  
Regulatory Mechanisms ◽  
Neuroendocrine Control ◽  
Complex Interactions ◽  
Development And Differentiation ◽  
Growth Metabolism

Reproduction is one of the important physiological events for the maintenance of the species. Hormonal and neuroendocrine regulation of teleost requires multiple and complex interactions along the hypothalamic-pituitary-gonad (HPG) axis. Within this axis, gonadotropin-releasing hormone (GnRH) regulates the synthesis and release of gonadotropins, follicle-stimulating hormone (FSH), and luteinizing hormone (LH). Steroidogenesis drives reproduction function in which the development and differentiation of gonads. In recent years, new neuropeptides have become the focus of reproductive physiology research as they are involved in the different regulatory mechanisms of these species' growth, metabolism, and reproduction. However, especially in fish, the role of these neuropeptides in the control of reproductive function is not well studied. The study of hormonal and neuroendocrine events that regulate reproduction is crucial for the development and success of aquaculture.

scholarly journals Role of Kisspeptin in Puberty in Humans

2020 ◽  
pp. 92-97
Author(s):  
Ravi Kant ◽  
Mahendra Kumar Meena
Keyword(s):  
Reproductive Biology ◽  
Conventional Treatment ◽  
Hypogonadotropic Hypogonadism ◽  
Follicle Stimulating Hormone ◽  
Gonadotropin Releasing Hormone ◽  
Pilot Studies ◽  
Releasing Hormone ◽  
Infertile Couples ◽  
Stimulating Hormone

Kisspeptin or GPR-54 is a product of KISS 1 gene regulating the production of gonadotropin releasing hormone (GnRH), luteinizing (LH) as well follicle stimulating hormone (FSH). Both LH and FSH are important hormones for reproduction in animals as well in humans. The recognition of Kisspeptin has a landmark bearing in reproductive biology. Few recent pilot studies have convincingly proven it to be a promising molecule in treating infertile couples especially those having hypogonadotropic hypogonadism not responding to conventional treatment.

scholarly journals Obligatory role of hypothalamic neuroestradiol during the estrogen-induced LH surge in female ovariectomized rhesus monkeys

2017 ◽  
Vol 114 (52) ◽  
pp. 13804-13809 ◽  
Author(s):  
Brian P. Kenealy ◽  
Kim L. Keen ◽  
James P. Garcia ◽  
Lucille K. Kohlenberg ◽  
Ei Terasawa
Keyword(s):  
Positive Feedback ◽  
Rhesus Monkeys ◽  
Feedback Loop ◽  
Reproductive Function ◽  
Feedback Mechanism ◽  
Gonadotropin Releasing Hormone ◽  
Feedback Effects ◽  
17Β Estradiol ◽  
Positive Feedback Mechanism

Negative and positive feedback effects of ovarian 17β-estradiol (E2) regulating release of gonadotropin releasing hormone (GnRH) and luteinizing hormone (LH) are pivotal events in female reproductive function. While ovarian feedback on hypothalamo–pituitary function is a well-established concept, the present study shows that neuroestradiol, locally synthesized in the hypothalamus, is a part of estrogen’s positive feedback loop. In experiment 1, E2 benzoate-induced LH surges in ovariectomized female monkeys were severely attenuated by systemic administration of the aromatase inhibitor, letrozole. Aromatase is the enzyme responsible for synthesis of E2 from androgens. In experiment 2, using microdialysis, GnRH and kisspeptin surges induced by E2 benzoate were similarly attenuated by infusion of letrozole into the median eminence of the hypothalamus. Therefore, neuroestradiol is an integral part of the hypothalamic engagement in response to elevated circulating E2. Collectively, we will need to modify the concept of estrogen’s positive feedback mechanism.

scholarly journals The role of the adiponectin system in acute fasting-impaired mouse ovaries

Reproduction ◽  
2019 ◽  
Vol 158 (5) ◽  
pp. 429-440
Author(s):  
Yingying Han ◽  
Shuhao Zhang ◽  
Haotong Zhuang ◽  
Sijie Fan ◽  
Jiayi Yang ◽  
...  
Keyword(s):  
Energy Homeostasis ◽  
Follicle Stimulating Hormone ◽  
Reproductive Function ◽  
Acute Malnutrition ◽  
Physiological Status ◽  
Normal Female ◽  
Fat Depots ◽  
Stimulating Hormone

Adiponectin (ADIPOQ, encoded by Adipoq) is an important white adipose-derived adipokine linked to energy homeostasis and reproductive function. This study aims to reveal the expression and role of the adiponectin system in the ovaries under acute malnutrition. In this study, 48-h food deprivation significantly inhibited ovarian growth by suppressing cell proliferation and inducing cell apoptosis in the ovaries of gonadotrophin-primed immature mice. It was also accompanied by significantly decelerated basic metabolism (glucose, triacylglycerol and cholesterol), varied steroid hormones (follicle-stimulating hormone, luteinizing hormone and estradiol) and vanishment of the peri-ovarian fat. It is noteworthy that after acute fasting, the adiponectin levels in ovaries rather than in blood were significantly elevated. Immunohistochemical study demonstrated that adiponectin and its receptors (ADIPOR1 and ADIPOR2) primarily appeared in ovarian somatic and/or germ cells, and their protein expressions were upregulated in the ovaries from fasted mice. Further in vitro study verified that ADIPOR1/2 agonist obviously inhibited follicle-stimulating hormone-induced oocyte meiotic resumption, while the antagonist significantly enhanced the percentage of oocyte maturation in the absence of follicle-stimulating hormone. Furthermore, the build up of peri-ovarian fat under physiological status in mice showed a positive correlation with both the hypertrophy of adipocytes and growth of ovaries. Taken together, these findings indicate that the upregulation of the adiponectin system disturbs the normal female reproductive function under the malnutrition status, and it may be associated with the loss of peri-ovarian fat depots.

Evidence for cAMP as a mediator of gonadotropin secretion from male pituitaries

1987 ◽  
Vol 253 (3) ◽  
pp. E296-E299
Author(s):  
G. A. Bourne ◽  
D. M. Baldwin
Keyword(s):  
Protein Synthesis ◽  
Potential Role ◽  
De Novo ◽  
Follicle Stimulating Hormone ◽  
Gonadotropin Releasing Hormone ◽  
Dibutyryl Camp ◽  
Camp Production ◽  
Gonadotropin Secretion ◽  
De Novo Protein Synthesis

The purpose of this study was to use sodium flufenamate, a compound that inhibits gonadotropin-releasing hormone (GnRH)-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) production in the pituitary, to evaluate the potential role of cAMP as a mediator of GnRH-stimulated gonadotropin secretion from male pituitaries. Quartered male pituitaries were perifused at 37 degrees C and sequential effluent fractions collected every 10 min. Infusions of GnRH resulted in a twofold increase in luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. Cycloheximide, 5 microM, completely inhibited the GnRH-stimulated LH and FSH secretion. Infusions of 0.1 mM flufenamate had similar effects on gonadotropin secretion as cycloheximide, whereas the administration of 5 mM dibutyryl cAMP in combination with GnRH and flufenamate restored the secretory responses of both hormones. The flufenamate-inhibited GnRH stimulated LH and FSH release, which was restored by DBcAMP and appeared to be protein synthesis dependent and specific for cAMP. These results suggest an indirect role for cAMP as a mediator of gonadotropin secretion from male pituitaries. However, in contrast to female pituitaries, the secretion of these hormones from male pituitaries is completely dependent on cAMP and de novo protein synthesis.

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