Publications
194 results found
jayasena C, abbara A, comninos A, et al., 2016, Novel circulating placental markers prokineticin-1, soluble fms-like tyrosine kinase-1, soluble endoglin and placental growth factor and risk of late miscarriage, Human Reproduction, Vol: 31, Pages: 2681-2688, ISSN: 0268-1161
STUDY QUESTION Are novel circulating placental markers prokineticin-1 (PK-1), soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng) and placental growth factor (PlGF) associated with late miscarriage in asymptomatic first trimester pregnant women?SUMMARY ANSWER Increased serum sFlt-1 or PlGF, but not sEng or PK-1, were significantly associated with reduced miscarriage risk after adjustment for age, BMI, gestational age, smoking and blood pressure.WHAT IS KNOWN ALREADY Abnormal placental development is observed in two-thirds of miscarriages. Identifying women at high risk of late miscarriage could help diagnose potentially treatable causes of miscarriage such as infection, thrombosis or immunological disease. Recently, the circulating placental markers PK-1, sFlt-1, sEng and PlGF have been identified; however, it is not known if circulating levels of these markers are associated with late miscarriage.STUDY DESIGN, SIZE, DURATION A single-centre observational cohort study with prospectively collected data was carried out at a tertiary care centre 2010–2012, in 993 asymptomatic pregnant women. Plasma PK-1, and serum sEng, sFlt-1 and PlGF were measured once in each patient during the antenatal booking visit, and pregnancy outcome was monitored prospectively. Less than 1% of patients were lost to follow-up. Multiples of median (MOM) levels were calculated to adjust for gestational age.PARTICIPANTS/MATERIALS, SETTING, METHODS Nine-hundred and ninety-three asymptomatic pregnant women attending antenatal clinic for a routine booking antenatal appointment were recruited to the study, of whom 12 were lost to follow-up and excluded from analysis. Of the cohort, 50 of the remaining 981 women suffered late miscarriage.MAIN RESULTS AND THE ROLE OF CHANCE Gestation-adjusted sEng, sFlt-1 and PlGF levels were 11% (P < 0.01), 36% (P < 0.001) and 30% (P < 0.001), respectively, lower in women who later suffered miscarriage compared with unaffected pregnanc
Dwyer AA, Jayasena CN, Quinton R, 2016, Congenital hypogonadotropic hypogonadism: implications of absent mini-puberty, Minerva Endocrinologica, Vol: 41, Pages: 188-195, ISSN: 1827-1634
The phenomenon known as "mini-puberty" refers to activation of the neonatal hypothalamo-pituitary axis causing serum concentrations of gonadotrophins and testosterone (T) to approach adult male levels. This early neonatal period is a key proliferative window for testicular germ cells and immature Sertoli cells. Although failure to spontaneously initiate (adolescent) puberty is the most evident consequence of a defective gonadotropin-releasing hormone (GnRH) neurosecretory network, absent mini-puberty is also likely to have a major impact on the reproductive phenotype of men with congenital hypogonadotrophic hypogonadism (CHH). Furthermore, the phase of male mini-puberty represents a key window-of-opportunity to identify congenital GnRH deficiency (either isolated CHH, or as part of combined pituitary hormone deficiency) in childhood. Among male neonates exhibiting "red flag" indicators for CHH (i.e. maldescended testes with or without cryptorchidism) a single serum sample (between 4-8 weeks of life) can pinpoint congenital GnRH deficiency far more rapidly and with much greater accuracy than dynamic tests performed in later childhood or adolescence. Potential consequences for missing absent mini-puberty in a male neonate include the lack of monitoring of pubertal progression/lack of progression, and the missed opportunity for early therapeutic intervention. This article will review our current understanding of the mechanisms and clinical consequences of mini-puberty. Furthermore, evidence for the optimal clinical management of patients with absent mini-puberty will be discussed.
Narayanaswamy S, Prague J, Jayasena C, et al., 2016, Investigating the KNDy hypothesis in humans by co-administration of kisspeptin, neurokinin B and naltrexone in men, Journal of Clinical Endocrinology & Metabolism, Vol: 101, Pages: 3429-3436, ISSN: 1945-7197
Context: A subpopulation of hypothalamic neurons co-localise three neuropeptides namely kisspeptin, neurokinin B (NKB) and dynorphin collectively termed KNDy neurons. Animal studies suggest they interact to affect pulsatile GnRH release (KNDy hypothesis); kisspeptin stimulates, NKB modulates and dynorphin (an opioid) inhibits. Objective: To investigate the KNDy hypothesis in humans, we assessed for the first time the effects of co-administration of kisspeptin-54, NKB and an opioid receptor antagonist, naltrexone on LH pulsatility (surrogate marker for GnRH pulsatility) and gonadotropin release. Design, setting and participants: Ethically approved prospective, single-blinded placebo-controlled study. Healthy male volunteers (n=5/group) attended our research facility for 8 study visits. Intervention and main outcome measure: After 1h baseline blood sampling, participants received a different intervention at each visit: oral 50mg naltrexone (NAL), 8h intravenous infusions of vehicle, 2.56nmol/kg/h NKB (NKB), 0.1nmol/kg/h kissspeptin-54 (KP) alone and in combination. Frequent blood sampling to measure plasma gonadotropins and sex steroids was conducted and LH pulsatility was determined using blinded deconvolution analysis. Results: All kisspeptin and naltrexone containing groups potently increased LH and LH pulsatility (p<0.001 vs vehicle). NKB alone did not affect gonadotropins. NKB+KP had significantly lower increases in gonadotropins compared with kisspeptin alone (p<0.01). NAL+KP was the only group to significantly increase LH pulse amplitude (p<0.001 vs vehicle).Conclusions: Our results suggest significant interactions between the KNDy neuropeptides on LH pulsatility and gonadotropin release in humans. This has important implications for improving our understanding of GnRH pulse generation in humans.
Thomas J, Radia U, Ramsay J, et al., 2016, Microdissection testicular sperm extraction for men undergoing cancer treatment, Expert Review of Quality of Life in Cancer Care, Vol: 1, Pages: 207-212, ISSN: 2380-9000
Steady improvements in the long term outlook for adolescents and young adults with cancer require a shift in focus towards ensuring quality of life after cancer treatment as well as quantity. An important component of quality of life for many men is the ability to father a biological child. However, direct effects of malignancy, as well as potentially gonadotoxic cancer treatments, render many men azoospermic. Where cryopreservation of a good quality semen sample is not possible or was not offered prior to initiation of treatment, microdissection testicular sperm extraction (mTESE) offers a potential route to biological fatherhood. This review explores current evidence supporting the use of mTESE in patients treated for cancer, as well as some of the barriers and questions that still remain before this technique can form part of routine practice.
Narayanaswamy S, Jayasena CN, Ng N, et al., 2015, Subcutaneous infusion of kisspeptin-54 stimulates gonadotrophin release in women and the response correlates with basal oestradiol levels, Clinical Endocrinology, Vol: 84, Pages: 939-945, ISSN: 1365-2265
Background and objective: Kisspeptin stimulates hypothalamic GnRH secretion resulting in gonadotrophin release and has potential as a future therapeutic. Chronic subcutaneous infusion of kisspeptin via a pump (similar to an insulin pump) may provide an alternative route of administration in the future. We investigated for the first time in humans, the gonadotrophin response to subcutaneous (SC) infusions of kisspeptin-54 in healthy women. Women are markedly more responsive to exogenous kisspeptin in the late follicular phase pre-ovulation when oestradiol levels are naturally high. Therefore we further investigated whether there was a correlation between baseline oestradiol levels and LH response to kisspeptin. Design and patients: A prospective, single-blinded placebo-controlled study. Healthy women (n=4) received an 8 hour SC infusion of kisspeptin-54 0.1, 0.3 or 1.0nmol/kg/h or saline in the early follicular phase of 4 separate menstrual cycles. Gonadotrophins and oestradiol were measured every 10 minutes during the infusions. Results: SC infusion of kisspeptin-54 increased LH and FSH. The LH response to SC infusion of kisspeptin-54 (0.3 and 1.0nmol/kg/h) positively correlated with baseline oestradiol levels (p<0.001). Further statistical analyses showed that in the 1.0nmol/kg/h group a 100pmol/L rise in baseline oestradiol was associated with a 1.0 IU/L increase in LH.Conclusions: Kisspeptin administered via a SC infusion could be a viable future therapeutic route of administration for patients with infertility. Baseline oestradiol levels may be an important determinant of the gonadotropin response to kisspeptin treatment in women and should be taken into consideration when evaluating gonadotrophin response.
Patel A, Stroud T, Breen D, et al., 2015, Patient age predicts the delay before survivors of cancer utilise their cryopreserved sperm for assisted reproductive technology., Blood, Vol: 126, Pages: 4481-4481, ISSN: 0006-4971
Objective: Sperm cryopreservation (sperm banking) is the recommended standard of care for fertility preservation for men with cancer. Men can utilise their sperm for assisted reproductive technology (ART) when they are ready to become fathers. However, the duration of sperm cryopreservation that should be offered to men is unknown. We hypothesised that younger men with cancer require a longer duration of sperm storage before readiness to utilise their samples for ART, compared with older patients. To test this hypothesis, we investigated whether age at sperm harvest predicts the time of sperm storage necessary before ART.Design: A retrospectively analysed cohort study spanning 37 years using prospectively acquired routine clinical data.Setting: A specialist andrology facility in the UK, that provides unlimited storage of sperm as part of NHS treatment free-of-charge to the patient.Participants: Adolescent boys and men with a confirmed diagnosis of cancer were identified by cross-referencing and verifying patient records: Human Fertility & Embryology Authority (HEFA), Department of Andrology, and the NHS Spine Services Portal database, part of the Health and Social Care Information Centre.Main outcome measures: The primary outcome measures were the effect of age on the time from sperm cryopreservation to use for ART, and the specificity and sensitivity of age at predicting the requirement of >10 years sperm storage.Results: 4305 men harvested and cryopreserved their sperm between 1976 and 2013. Men with cancer comprised 3191 and were included in the study. The cancer types that indicated sperm cryopreservation comprised testicular (1130, 35.4%), lymphoma (762, 23.9%), leukaemia (462, 14.5%), and others (838, 26.3%). At sperm harvesting, their median age was 30.3 years (IQR 24.6 to 36.2). Sperm from 217 (6.8%) patients with a median age of 31.3 (IQR 26.5 to 36.7) were utilized for ART after a median of 7.8 years (interquartile range (IQR) 3.5 to 14.3).Increasin
Abbara A, Jayasena CN, Christopoulos G, et al., 2015, Efficacy of kisspeptin-54 to trigger oocyte maturation in women at high risk of OHSS during IVF therapy, Journal of Clinical Endocrinology and Metabolism, Vol: 100, Pages: 3322-3331, ISSN: 0368-1610
Context:In Vitro Fertilization (IVF) treatment is an effective therapy for infertility, but can result in the potentially life-threatening complication ‘ovarian hyperstimulation syndrome’ (OHSS).Objective:To investigate whether kisspeptin-54 can be used to effectively and safely trigger oocyte maturation in women undergoing IVF treatment at high risk of developing OHSS.Design:Phase 2 multi-dose open label randomized clinical trial carried out during 2013–2014.Setting:Hammersmith Hospital IVF unit, London, UK.Patients:Sixty women at high risk of developing OHSS Intervention:Following a standard recombinant FSH/GnRH antagonist protocol, patients were randomized to receive a single injection of kisspeptin-54 to trigger oocyte maturation using an adaptive design for dose allocation (3.2nmol/kg, n=5; 6.4nmol/kg, n=20; 9.6nmol/kg, n=15; 12.8nmol/kg, n=20). Oocytes were retrieved 36hrs after kisspeptin-54 administration, assessed for maturation, and fertilized by intra-cytoplasmic sperm injection (ICSI) with subsequent transfer of one or two embryos. Women were routinely screened for the development of OHSS.Main Outcome Measure:Oocyte maturation was measured by oocyte yield (percentage of mature oocytes retrieved from follicles ≥14mm on ultrasound). Secondary outcomes include rates of OHSS and pregancy. Results:Oocyte maturation occurred in 95% of women. Highest oocyte yield (121%) was observed following 12.8nmol/kg kisspeptin-54, which was +69% (CI -16%,+153%) greater than following 3.2nmol/kg. At all doses of kisspeptin-54, biochemical pregnancy, clinical pregnancy and live birth rates per transfer (n=51) were 63%, 53% and 45%, respectively. Highest pregnancy rates were observed following 9.6nmol/kg kisspeptin-54 (85%, 77% and 62%, respectively). No woman developed moderate, severe or critical OHSS.Conclusion:Kisspeptin-54 is a promising approach to effectively and safely trigger oocyte
Clarke H, Dhillo WS, Jayasena CN, 2015, Comprehensive Review on Kisspeptin and Its Role in Reproductive Disorders, Endocrinology and Metabolism, Vol: 30, Pages: 124-141, ISSN: 2093-5978
Kisspeptin has recently emerged as a key regulator of the mammalian reproductive axis. It is known that kisspeptin, acting centrally via the kisspeptin receptor, stimulates secretion of gonadotrophin releasing hormone (GnRH). Loss of kisspeptin signaling causes hypogonadotrophic hypogonadism in humans and other mammals. Kisspeptin interacts with other neuropeptides such as neurokinin B and dynorphin, to regulate GnRH pulse generation. In addition, a growing body of evidence suggests that kisspeptin signaling be regulated by nutritional status and stress. Kisspeptin may also represent a novel potential therapeutic target in the treatment of fertility disorders. Early human studies suggest that peripheral exogenous kisspeptin administration stimulates gonadotrophin release in healthy adults and in patients with certain forms of infertility. This review aims to concisely summarize what is known about kisspeptin as a regulator of reproductive function, and provide an update on recent advances within this field.
Jayasena CN, Abbara A, Narayanaswamy S, et al., 2015, Direct comparison of the effects of intravenous kisspeptin-10, kisspeptin-54 and GnRH on gonadotrophin secretion in healthy men, Human Reproduction, Vol: 30, Pages: 1934-1941, ISSN: 1460-2350
study question: How potently does the novel hypothalamic stimulator of reproduction, kisspeptin, increase gonadotrophin secretionwhen compared with GnRH in healthy men?summaryanswer: At the doses tested, intravenous administration of either of two major kisspeptin isoforms, kisspeptin-10 and -54, wasassociated with similar levels of gonadotrophin secretion in healthy men; however, GnRH was more potent when compared with either kisspeptinisoform.what is known already: Kisspeptin-10 and -54 are naturally occurring hormones in the kisspeptin peptide family which potently stimulatesendogenous GnRH secretion from the hypothalamus, so have the potential to treat patients with reproductive disorders. Rodent studiessuggest that kisspeptin-54 is more potent when compared with kisspepitn-10; however, their effects have not previously been directly comparedin humans, or compared with direct pituitary stimulation of gonadotrophin secretion using GnRH.study design, size and duration: A single-blinded placebo controlled physiological study was performed from January to December2013. Local ethical approval was granted, and five participants were recruited to each dosing group.participants/materials, setting, methods: Healthy men were administered vehicle, kisspeptin-10, kisspeptin-54 andGnRH intravenously for 3 h on different study days. Each hormone was administered at 0.1, 0.3 and 1.0 nmol/kg/h doses (n ¼ 5 subjects pergroup). Regular blood sampling was conducted throughout the study to measure LH and FSH. Study visits were conducted at least a week apart.main results and the role of chance: Serum LH and FSH levels were 3-fold higher during GnRH infusion when comparedwith kisspeptin-10 and 2-fold higher when compared with kisspeptin-54 [mean area under the curve serum LH during infusion (in hours timesinternational units per litre, h.IU/l): 10.81+1.73, 1.0 nmol/kg/h kisspeptin-10; 14.43+1.27, 1.0 nmol/kg/h kisspeptin-54; 34.06+5.18,1.0 nmol/kg/h GnRH, P , 0.001 versus kis
Abbara A, Jayasena CN, Christopoulos G, et al., 2015, Kisspeptin-54 safely and effectively triggers oocyte maturation in women at high risk of the ovarian hyperstimulation syndrome (OHSS), 31st Annual Meeting of the European-Society-of-Human-Reproduction-and-Embryology (ESHRE), Publisher: OXFORD UNIV PRESS, Pages: 68-68, ISSN: 0268-1161
Jayasena CN, Comninos AN, Narayanaswamy S, et al., 2015, The identification of elevated urinary kisspeptin-immunoreactivity during pregnancy, ANNALS OF CLINICAL BIOCHEMISTRY, Vol: 52, Pages: 395-398, ISSN: 0004-5632
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Comninos AN, Anastasovska J, Sahuri-Arisoylu M, et al., 2015, Kisspeptin signaling in the amygdala modulates reproductive hormone secretion, Brain Structure & Function, Vol: 221, Pages: 2035-2047, ISSN: 1863-2661
Kisspeptin (encoded by KISS1) is a crucial activator of reproductive function. The role of kisspeptin has been studied extensively within the hypothalamus but little is known about its significance in other areas of the brain. KISS1 and its cognate receptor are expressed in the amygdala, a key limbic brain structure with inhibitory projections to hypothalamic centers involved in gonadotropin secretion. We therefore hypothesized that kisspeptin has effects on neuronal activation and reproductive pathways beyond the hypothalamus and particularly within the amygdala. To test this, we mapped brain neuronal activity (using manganese-enhanced MRI) associated with peripheral kisspeptin administration in rodents. We also investigated functional relevance by measuring the gonadotropin response to direct intra-medial amygdala (MeA) administration of kisspeptin and kisspeptin antagonist. Peripheral kisspeptin administration resulted in a marked decrease in signal intensity in the amygdala compared to vehicle alone. This was associated with an increase in luteinizing hormone (LH) secretion. In addition, intra-MeA administration of kisspeptin resulted in increased LH secretion, while blocking endogenous kisspeptin signaling within the amygdala by administering intra-MeA kisspeptin antagonist decreased both LH secretion and LH pulse frequency. We provide evidence for the first time that neuronal activity within the amygdala is decreased by peripheral kisspeptin administration and that kisspeptin signaling within the amygdala contributes to the modulation of gonadotropin release and pulsatility. Our data suggest that kisspeptin is a ‘master regulator’ of reproductive physiology, integrating limbic circuits with the regulation of gonadotropin-releasing hormone neurons and reproductive hormone secretion.
Jayasena CN, Comninos AN, Stefanopoulou E, et al., 2015, Neurokinin B Administration Induces Hot Flushes in Women, SCIENTIFIC REPORTS, Vol: 5, ISSN: 2045-2322
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- Citations: 70
Jayasena CN, Izzi-Engbeaya C, Narayanaswamy S, et al., 2015, Associations of coefficient of variation of serum GH with previous radiotherapy, hypopituitarism and cardiac disease in patients with treated acromegaly, Clinical Endocrinology, Vol: 82, Pages: 870-875, ISSN: 0300-0664
Jayasena CN, Abbara A, Izzi-Engbeaya C, et al., 2014, Reduced Levels of Plasma Kisspeptin During the Antenatal Booking Visit Are Associated With Increased Risk of Miscarriage, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 99, Pages: E2652-E2660, ISSN: 0021-972X
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- Citations: 48
Jayasena CN, Comninos AN, Narayanaswamy S, et al., 2014, Acute and chronic effects of kisspeptin-54 administration on GH, prolactin and TSH secretion in healthy women, Clinical Endocrinology, Vol: 81, Pages: 891-898, ISSN: 1365-2265
Jayasena CN, Franks S, 2014, The management of patients with polycystic ovary syndrome, NATURE REVIEWS ENDOCRINOLOGY, Vol: 10, Pages: 624-636, ISSN: 1759-5029
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- Citations: 116
Jayasena CN, Abbara A, Comninos AN, et al., 2014, Kisspeptin-54 triggers egg maturation in women undergoing in vitro fertilization, Journal of Clinical Investigation, Vol: 124, Pages: 3667-3677, ISSN: 0021-9738
BACKGROUND. Patients with mutations that inactivate kisspeptin signaling are infertile. Kisspeptin-54, the major circulating isoform of kisspeptin in humans, potently stimulates reproductive hormone secretion in humans. Animal studies suggest that kisspeptin is involved in generation of the luteinizing hormone surge, which is required for ovulation; therefore, we hypothesized that kisspeptin-54 could be used to trigger egg maturation in women undergoing in vitro fertilization therapy.METHODS. Following superovulation with recombinant follicle-stimulating hormone and administration of gonadotropin-releasing hormone antagonist to prevent premature ovulation, 53 women were administered a single subcutaneous injection of kisspeptin-54 (1.6 nmol/kg, n = 2; 3.2 nmol/kg, n = 3; 6.4 nmol/kg, n = 24; 12.8 nmol/kg, n = 24) to induce a luteinizing hormone surge and egg maturation. Eggs were retrieved transvaginally 36 hours after kisspeptin injection, assessed for maturation (primary outcome), and fertilized by intracytoplasmic sperm injection with subsequent transfer of one or two embryos.RESULTS. Egg maturation was observed in response to each tested dose of kisspeptin-54, and the mean number of mature eggs per patient generally increased in a dose-dependent manner. Fertilization of eggs and transfer of embryos to the uterus occurred in 92% (49/53) of kisspeptin-54–treated patients. Biochemical and clinical pregnancy rates were 40% (21/53) and 23% (12/53), respectively.CONCLUSION. This study demonstrates that a single injection of kisspeptin-54 can induce egg maturation in women with subfertility undergoing in vitro fertilization therapy. Subsequent fertilization of eggs matured following kisspeptin-54 administration and transfer of resulting embryos can lead to successful human pregnancy.TRIAL REGISTRATION. ClinicalTrials.gov NCT01667406.FUNDING. Medical Research Council, Wellcome Trust, and National Institute for Health Research.
Comninos AN, Jayasena CN, Stefanopoulou E, et al., 2014, The hypothalamic hormone neurokinin B: a novel therapeutic target for menopausal hot flushes, 30th Annual Meeting of the European-Society-of-Human-Reproduction-and-Embryology (ESHRE), Publisher: OXFORD UNIV PRESS, Pages: 105-105, ISSN: 0268-1161
Abbara A, Jayasena CN, Comninos AN, et al., 2014, Kisspeptin - a novel physiological trigger for oocyte maturation in IVF treatment, 30th Annual Meeting of the European-Society-of-Human-Reproduction-and-Embryology (ESHRE), Publisher: OXFORD UNIV PRESS, Pages: 50-50, ISSN: 0268-1161
Jayasena CN, Abbara A, Veldhuis JD, et al., 2014, Increasing LH Pulsatility in Women With Hypothalamic Amenorrhoea Using Intravenous Infusion of Kisspeptin-54, Journal of Clinical Endocrinology and Metabolism, Vol: 99, Pages: E953-E961, ISSN: 0021-972X
Background:Hypothalamic amenorrhea (HA) is the one of the most common causes of period loss in women of reproductive age and is associated with deficient LH pulsatility. High-dose kisspeptin-54 acutely stimulates LH secretion in women with HA, but chronic administration causes desensitization. GnRH has paradoxical effects on reproductive activity; we therefore hypothesized that a dose-dependent therapeutic window exists within which kisspeptin treatment restores the GnRH/LH pulsatility in women with HA.Aim:The aim of the study was to determine whether constant iv infusion of kisspeptin-54 temporarily increases pulsatile LH secretion in women with HA.Methods:Five patients with HA each underwent six assessments of LH pulsatility. Single-blinded continuous iv infusion of vehicle or kisspeptin-54 (0.01, 0.03, 0.10, 0.30, or 1.00 nmol/kg/h) was administered. The LH pulses were detected using blinded deconvolution.Results:Kisspeptin increased LH pulsatility in all patients with HA, with peak responses observed at different doses in each patient. The mean peak number of pulses during infusion of kisspeptin-54 was 3-fold higher when compared with vehicle (number of LH pulses per 8 h: 1.6 ± 0.4, vehicle; 5.0 ± 0.5, kisspeptin-54, P < .01 vs vehicle). The mean peak LH pulse secretory mass during kisspeptin-54 was 6-fold higher when compared with vehicle (LH pulse secretory mass in international units per liter: 3.92 ± 2.31, vehicle; 23.44 ± 12.59, kisspeptin-54; P < .05 vs vehicle).Conclusions:Kisspeptin-54 infusion temporarily increases LH pulsatility in women with HA. Furthermore, we have determined the dose range within which kisspeptin-54 treatment increases basal and pulsatile LH secretion in women with HA. This work provides a basis for studying the potential of kisspeptin-based therapies to treat women with HA.
Comninos AN, Anastasovska J, Sahuri-Arisoylu M, et al., 2014, Kisspeptin Inhibits Neuronal Activity in the Amygdala of Male Mice, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X
Jayasena CN, Abbara A, Comninos AN, et al., 2014, Comparing the Effects of Pituitary Versus Hypothalamic Stimulation of the Human Reproductive Axis Using Equimolar Intravenous Infusions of Kisspeptin-10, Kisspeptin-54 and Gonadotrophin Releasing Hormone (GnRH) in Healthy Men, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X
Comninos AN, Jayasena CN, Stefanopoulou E, et al., 2014, Neurokinin B Administration Induces Menopausal-like Hot Flushes in Healthy Young Women, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X
Abbara A, Jayasena CN, Comninos AN, et al., 2014, Kisspeptin - a Novel Physiological Trigger for Oocyte Maturation in IVF Treatment, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X
Abbara A, Jayasena CN, Izzi-Engbeaya C, et al., 2014, Plasma Kisspeptin Measurement during Early Pregnancy Is a Highly Predictive Marker of Subsequent Miscarriage, Publisher: ENDOCRINE SOC, ISSN: 0163-769X
Mogford JT, Jayasena CN, Dhillo WS, 2014, Evaluating the potential utility of kisspeptin to treat reproductive disorders., Expert Rev Endocrinol Metab, Vol: 9, Pages: 251-261
The kisspeptins, encoded by the KISS1 gene, are a group of newly discovered peptides, which have been found to play an important regulatory role in human reproduction. Loss of function mutations of kisspeptin or the kisspeptin receptor have been shown to cause pubertal failure; whereas activating mutations cause precocious puberty. Central and peripheral administration of kisspeptin to mammals stimulates gonadotrophin secretion via gonadotrophin releasing hormone (GnRH) stimulation. Similar observations have been reported in human studies as well as an increase in luteinizing hormone (LH) pulsatility. Kisspeptin is now known to be associated with brain sexual differentiation, sexual dimorphism, pubertal initiation and sex steroids feedback loops, which will be discussed in this review. Metabolic state, stress, and other neuropeptides such as neurokinin B (NKB) are associated with changes in kisspeptin's stimulatory action. The conclusions from kisspeptin studies so far have led to the consideration of potential therapeutic applications, which will be discussed. Increasing our understanding of kisspeptin may aid our knowledge and management of infertility, contraception and hormone sensitive conditions.
Abbara A, Jayasena C, Comninos A, et al., 2014, Kisspeptin: a novel physiological trigger for oocyte maturation in in-vitro fertilisation treatment, LANCET, Vol: 383, Pages: 17-17, ISSN: 0140-6736
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Comninos A, Jayasena C, Nijher G, et al., 2014, The effects of kisspeptin administration on the menstrual cycle in healthy women, LANCET, Vol: 383, Pages: 37-37, ISSN: 0140-6736
Jayasena CN, Dhillo WS, Bloom SR, 2014, Does Kisspeptin signaling offer a new way to treat infertility?, Expert Review of Obstetrics & Gynecology, Vol: 4, Pages: 477-481, ISSN: 1747-4116
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