scholarly journals Effects of the Hormone Kisspeptin on Reproductive Hormone Release in Humans

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Joanne L. Calley ◽  
Waljit S. Dhillo
Keyword(s):  
Human Subjects ◽  
Reproductive Function ◽  
Current Data ◽  
Loss Of Function ◽  
Potential Therapeutic Role ◽  
Human Reproductive ◽  
Normal Human ◽  
Gonadotrophin Releasing Hormone ◽  
Research Avenue

The kisspeptins are a family of neuropeptides which act as upstream stimulators of gonadotrophin releasing hormone (GnRH) neurons. Kisspeptin signalling is prerequisite to establishing the normal human reproductive phenotype; loss of function mutations in the KISS1 or KISS1R gene produces normosmic hypogonadotrophic hypogonadism in humans and mice, whilst increased activation of KISS1R causes precocious puberty. Administration of exogenous kisspeptin to human subjects stimulates an acute gonadotrophin rise. Serum kisspeptin levels also markedly increase during pregnancy. The identification of kisspeptin has been one of the biggest discoveries in the field of reproductive endocrinology, since the isolation and sequencing of GnRH in 1977, and has generated a novel research avenue which has received much attention over the past decade. This research has delineated many properties of the KISS1-KISS1R system, but there is still further work to do. Understanding kisspeptin’s role throughout our reproductive lifetime should help us better understand—and therefore treat—disorders of reproductive function. Promisingly, the current data supports the potential to develop kisspeptin based therapies. As an outlook article this paper focusses predominantly on our groups recent investigations into the effects of kisspeptin administration to humans and the potential therapeutic role of kisspeptin.

scholarly journals The Expression of miRNAs in Human Ovaries, Oocytes, Extracellular Vesicles, and Early Embryos: A Systematic Review

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1564 ◽  
Author(s):  
Albert Salas-Huetos ◽  
Emma R. James ◽  
Kenneth I. Aston ◽  
Timothy G. Jenkins ◽  
Douglas T. Carrell ◽  
...  
Keyword(s):  
Systematic Review ◽  
Extracellular Vesicles ◽  
Mirna Expression ◽  
Observational Studies ◽  
Reproductive Function ◽  
Human Reproduction ◽  
Reproductive Tissues ◽  
Early Embryos ◽  
Human Reproductive

The recent discovery of microRNAs (miRNAs) in human reproductive tissues and cells indicates a possible functional role in reproductive function. However, the studies published to date in female reproductive tissues/cells and embryos are inconclusive and sometimes controversial. In order to update the knowledge of this field, the present study aimed to discuss, through a systematic review, the role of miRNAs in female human reproduction and early embryogenesis. We conducted a systematic review of the published literature in MEDLINE and EMBASE databases through June 2018 (plus a complementary search until July 2019), in accordance with the PRISMA guidelines. We have included descriptive and observational studies, in which fertile/infertile women were well-defined. The primary outcome was the miRNA expression in ovaries, oocytes, extracellular vesicles, and embryos. We identified 25,204 articles, of which 28 were selected for qualitative analysis: 18 in ovaries and extracellular vesicles, three in oocytes, and seven in embryos. The present systematic review of descriptive and observational studies demonstrates that aberrant miRNA expression in female reproductive tissues/cells and embryos is related with infertility and embryogenesis errors. The expression of specific miRNAs, particularly in extracellular vesicles, may be used in the future as biomarkers of infertility and prognostic tools of embryo development.

Initiation of migrating myoelectric complexes in human subjects: role of duodenal acidification and plasma motilin

1981 ◽  
Vol 59 (2) ◽  
pp. 173-179 ◽  
Author(s):  
E. E. Daniel ◽  
J. E. T. Fox ◽  
S. M. Collins ◽  
T. D. Lewis ◽  
M. Meghji ◽  
...  
Keyword(s):  
Human Subjects ◽  
Duodenal Bulb ◽  
Maximal Activity ◽  
Phase Iii ◽  
Motor Complex ◽  
Duodenal Acidification ◽  
Normal Human ◽  
Plasma Motilin ◽  
The Relationship

The hypothesis that acid, emptied intermittently from the stomach during fasting, might initiate the duodenal phase of the migrating motor complex was tested in normal human subjects, in addition, the relationship between plasma motilin concentrations and the initiation of migrating motor complexes was examined. Migrating complexes occurred spontaneously in the absence of acid in the duodenal bulb and in the presence of duodenal bulb neutralization with sodium bicarbonate. Thus duodenal bulb acidification is not necessary for initiation of the duodenal phase of the migrating motor complexes. Further-more, cyclical increases in plasma motilin concentrations were not closely correlated with the initiation of the gastric phase of maximal activity of the migrating motor complexes. However, motilin concentrations were decreased significantly following onset of the duodenal phase III. We conclude that neither duodenal acidification nor increases in motilin concentration are necessary to initiate migrating motor complexes in man.

scholarly journals Mouse models of altered gonadotrophin action: insight into male reproductive disorders

Reproduction ◽  
2014 ◽  
Vol 148 (4) ◽  
pp. R63-R70 ◽  
Author(s):  
Kim C Jonas ◽  
Olayiwola O Oduwole ◽  
Hellevi Peltoketo ◽  
Susana B Rulli ◽  
Ilpo T Huhtaniemi
Keyword(s):  
Mouse Models ◽  
Molecular Mechanisms ◽  
Pituitary Hormones ◽  
Loss Of Function ◽  
Reproductive Disorders ◽  
Human Reproductive ◽  
Multiple Loss ◽  
The Relationship

The advent of technologies to genetically manipulate the mouse genome has revolutionised research approaches, providing a unique platform to study the causality of reproductive disorders in vivo. With the relative ease of generating genetically modified (GM) mouse models, the last two decades have yielded multiple loss-of-function and gain-of-function mutation mouse models to explore the role of gonadotrophins and their receptors in reproductive pathologies. This work has provided key insights into the molecular mechanisms underlying reproductive disorders with altered gonadotrophin action, revealing the fundamental roles of these pituitary hormones and their receptors in the hypothalamic–pituitary–gonadal axis. This review will describe GM mouse models of gonadotrophins and their receptors with enhanced or diminished actions, specifically focusing on the male. We will discuss the mechanistic insights gained from these models into male reproductive disorders, and the relationship and understanding provided into male human reproductive disorders originating from altered gonadotrophin action.

scholarly journals SUN-253 PROKR2 Neurons of the Amygdalohippocampal Area in Reproductive Function

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Brenda Cisneros Larios ◽  
Carol F Elias
Keyword(s):  
Steroid Receptors ◽  
Reproductive Function ◽  
Sexually Dimorphic ◽  
Male Mice ◽  
Loss Of Function ◽  
Exposure Test ◽  
Male And Female ◽  
Female Mice ◽  
Reproductive Control

Abstract Kallmann Syndrome (KS) is characterized by infertility and anosmia due to deficiency in gonadotropin releasing hormone (GnRH) neuronal migration and olfactory bulb dysgenesis. Genetic studies have revealed that KS is caused by loss-of-function mutations in several genes including the prokineticin receptor 2 (PROKR2) gene (Abreu et al., 2008, Hardelin & Dode 2008). Mice with global deletion of Prokr2 replicate the phenotype of KS patients (Ng et al., 2005, Matsumoto et al., 2006). Whereas the role of PROKR2 during development is defined, little is known about PROKR2 neurons in adult reproduction. PROKR2 mRNA are highly expressed in reproductive control sites of the adult mouse brain (Cheng et al., 2006). Previous studies in our lab found PROKR2 mRNA and Prokr2-Cre GFP+ cells highly expressed in the amygdalohippocampal area (AHi, also called posterior nucleus of the amygdala) in a sexually-dimorphic pattern. Male mice have higher PROKR2 expression in the AHi compared to female mice (Mohsen et al., 2017). The amygdala is an important site of socio-sexual inputs and reproductive neuroendocrine responses in rodents and primates, including humans. We hypothesize Prokr2-Cre neurons in the AHi have a role in both male and female reproductive function. Using genetic tracing techniques, we mapped AHi Prokr2-Cre neuronal projections in both male and female mice and found dense innervation to reproductive control sites such as the medial preoptic area and the ventral premammillary nucleus in a sexually dimorphic pattern. A soiled bedding exposure test in sexually experienced male mice showed that an estimated 45% of cFos + cells in the AHi express Prokr2-Cre GFP. Dense sex steroid receptors expression was observed in AHi Prokr2-Cre GFP neurons of both male and female mice. Our preliminary data suggests AHi Prokr2-Cre neurons have a reproductive function in male and potentially also in female mice. Future studies will focus on selective activation and inhibition of these neurons using chemogenetic technology to determine putative inputs to brain sites that control the hypothalamo-pituitary-gonadal axis. We expect our studies will contribute to the understanding of the role of PROKR2 neurons in adult reproduction and reproductive deficits associated with PROKR2 mutations.

Role of molecular signaling pathways in the pathogenesis of adenomyosis

2021 ◽  
Vol 70 (3) ◽  
pp. 121-134
Author(s):  
Maria A. Shalina ◽  
Maria I. Yarmolinskaya ◽  
Elena A. Netreba ◽  
Alexandra K. Beganova
Keyword(s):  
Drug Therapy ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Transforming Growth Factor ◽  
Reproductive Function ◽  
Current Data ◽  
Diagnostic Methods ◽  
Molecular Signaling ◽  
Non Invasive

The prevalence of genital endometriosis and adenomyosis, in particular, is tending to increase. The lack of a complete understanding of the pathogenetic mechanisms and multifactorial causes of adenomyosis, the low effectiveness of existing drug therapy, and the importance of preserving reproductive function make it necessary to further study the pathogenesis of the disease, search for new non-invasive highly informative diagnostic methods and develop a new strategy for pathogenically based drug therapy. The review presents current data on the role of signaling pathways in the pathogenesis of the development of adenomyosis based on domestic and foreign literature sources retrieved from the electronic databases PubMed, CyberLeninka, and Google Scholar in the period from 1999 to 2020. Considerable emphasis is placed on the discussion of the research results in recent years. Based on the analysis, the role of transforming growth factor (TGF), vascular endothelial growth factor (VEGF), dual-specificity protein phosphatase (PTEN), Notch receptors, and eukaryotic translation initiation factors (eIFs) in the signaling of adenomyosis is presented. Further advanced study of signaling pathways in the pathogenesis of adenomyosis will allow developing highly specific and highly sensitive markers for non-invasive diagnostics, as well as new directions for drug treatment of the disease.

Epinephrine increases plasma immunoreactive atrial natriuretic hormone levels in humans

1987 ◽  
Vol 252 (6) ◽  
pp. E740-E745 ◽  
Author(s):  
J. A. Sanfield ◽  
Y. Shenker ◽  
R. J. Grekin ◽  
S. G. Rosen
Keyword(s):  
Heart Rate ◽  
Human Subjects ◽  
Beta Adrenergic ◽  
Natriuretic Hormone ◽  
Adrenergic Mechanisms ◽  
Adrenergic Antagonist ◽  
Normal Human ◽  
Atrial Natriuretic Hormone ◽  
Atrial Natriuretic

Six normal human subjects each underwent sequential 80-min infusions of saline and epinephrine (EPI) at 0.55 and 2.75 micrograms X min-1 X m-2 to determine the role of EPI in the control of atrial natriuretic hormone (ANH) in humans. Plasma immunoreactive-ANH (IR-ANH) levels nearly doubled in response to the infusion of EPI at 0.55 microgram X min-1 X m-2 (P less than 0.05) and then plateaued; heart rate accelerated significantly (P less than 0.01) with increasing plasma EPI levels, whereas systolic blood pressure increased only with higher plasma EPI levels (P less than 0.05). To determine whether beta-adrenergic mechanisms mediate the EPI-induced increase in IR-ANH, six additional subjects each received infusions on two separate days of saline for 240 min and the beta-adrenergic antagonist propranolol followed by propranolol plus EPI at 2.75 micrograms X min-1 X min-2 each for 80 min. Neither saline nor propranolol plus EPI caused a significant increase in plasma IR-ANH. We conclude that EPI increases plasma IR-ANH through beta-adrenergic mechanisms in humans. beta-Adrenergic-mediated increases in plasma IR-ANH levels appear to be unrelated to changes in the heart rate.

Role of Food Intake in the Modulation of Hexarelin-Induced Growth Hormone Release in Normal Human Subjects

2000 ◽  
Vol 32 (04) ◽  
pp. 152-156 ◽  
Author(s):  
L. De Marinis ◽  
A. Mancini ◽  
D. Valle ◽  
D. Izzi ◽  
A. Bianchi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Food Intake ◽  
Human Subjects ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Normal Human

scholarly journals Studies on the role of cephalic-vagal stimulation in the acid secretory response to eating in normal human subjects.

1977 ◽  
Vol 60 (2) ◽  
pp. 435-441 ◽  
Author(s):  
C T Richardson ◽  
J H Walsh ◽  
K A Cooper ◽  
M Feldman ◽  
J S Fordtran
Keyword(s):  
Vagal Stimulation ◽  
Human Subjects ◽  
Secretory Response ◽  
Normal Human
Sign in / Sign up

Export Citation Format

Share Document