Kisspeptins in human reproduction—future therapeutic potential

Kaur, Kulvinder Kochar; Allahbadia, Gautam N.; Singh, Mandeep

doi:10.1007/s10815-012-9856-1

Cited by 8 publications

(5 citation statements)

References 134 publications

(151 reference statements)

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“…On detailed analysis of families having knowledge ,it was demonstrated that in cases of normosmic HH, which is a monogenic mendelian disease there is an involvement of 6 genes namely GnRH1 [36,37], Gn RH R [26,38-,39], KISS1R [40][41], KISS1 [42,43] reviewed in kkk] TAC3 and its receptor TAC3R [44,]. Animal model studies have given a better understanding regarding the role of these factors in the gonadotropic axis [33,44].…”

Section: Hypogonadotropic Hypogonadismmentioning

confidence: 99%

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An Update on Aetiopathology, Various Genetic Causes and Management of Delayed Puberty-A Minireview

2019

JPNB

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Delayed Puberty (DP), especially in boys, is a common presentation in paediatrics. By definition DP is defined as the presentation of clinical signs of puberty 2-2.5SD later than in the normal population. With the recent advances in understanding of the neuroendocrine, genetic and environmental factors controlling pubertal development it has become easier to understand the pathophysiology of DP. The discovery of kisspeptin signaling through its receptor identified neuroendocrine mechanisms controlling the gonadotropin releasing hormone (GnRH) pulse generator at the onset of puberty. Genetic mechanisms from single gene mutations to single nucleotide polymorphisms associated with DP are being identified. Environmental factors, including nutritional factors, besides endocrine disruptors, have been associated with the secular trends and abnormal timing of puberty. Inspite of these advances, the main question remains how to differentiate DP associated with underlying pathology of hypogonadism from constitutional delay in growth and puberty (CDP) that remains challenging as biochemical tests do not always discriminate the 2.The diagnostic accuracies of newer investigations which include the 36-hour luteininzing hormone releasing hormone(LHRH) tests, GnRH agonist tests, antimullerian hormone and inhibin B, need further evaluation. Sex hormone replacement remains the main therapy that is available for DP, whose choice is based on clinical practice and the availability of the various sex steroid preparations. Spontaneous reversal of hypogonadism has been reported in boys having idiopathic hypogonadotropic hypogonadism following sex steroid treatment, which highlights the importance of reassessment at the end of pubertal induction .Novel therapies having a more physiological bases like gonadotropins or kisspeptin agonists are getting investigated for the management of hypogonadotropic hypogonadism. A careful assessment and knowledge of the normal physiology remains the mainstay of managing patients with DP.

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Section: Hypogonadotropic Hypogonadismmentioning

confidence: 99%

“…Since this is costly all patients might not afford it [83,84]. Recently Kp agonists have been tried in some cases having KISS1/KISS1R mutations [43,85] although not available in every country. Although NKB is not effective it being downstream of KISS, KP agonists are also effective in TAC3/TAC3R mutations [86][87][88].…”

Section: Fertility Treatmentmentioning

confidence: 99%

An Update on Aetiopathology, Various Genetic Causes and Management of Delayed Puberty-A Minireview

2019

JPNB

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“…This peptide can get further hydrolyzed into a number of truncated fragments; kisspeptin 54(Kp54/metastin with 54 amino acids), kisspeptin 14(14 amino acids) and Kp13 and Kp10 with 13and 10 amino acids respectively. 1,2 Initially kisspeptin 54 got named metastin since it was isolated in metastatic tissues though both are synonymous fragments encoded by the same gene that encodes the larger peptide which then further gets broken into smaller fragments by enzymes. Then Jayasena et al 3 started studying them in human reproduction…”

Section: Commentarymentioning

confidence: 99%

Has Kisspeptin found a place to be a biomarker in the differentiation of viability of early pregnancy-a short commentary

Kaur¹,

Allahbadia²,

Singh³

2018

MOJCSR

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“…Further since Kp 10 is a potent stimulator of LH and increases pulse frequency in men and thereby LH and testosterone levels in normal men there may be a potential role of Kp agonists in HH due to KISS 1/KISS1R mutations ( [129], reviewed in [130]).…”

Section: Role Of Estradiol (In Male Chh)mentioning

confidence: 99%

Idiopathic Hypogonadotropic Hypogonadism— An Update on the Aetiopathogenesis, Management of IHH in Both Males and Females—An Exhaustive Review

Kulvinder¹,

Allahbadia²,

Singh³

2016

ASM

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Methods: Asystematic literature search was performed using PUBMED for all English articles up to April 2014. Although this review mainly focuses on published human studies, it also draws attention to where future research should be directed based on animal studies. Results: Besides the 9 known mutations widely quoted for KS namely KAL1, Fibroblast growth factor 8 (FGF8), fibroblast growth factor receptor 1 (FGFR1), prokineticin 2 (PROK2), PROK receptor 2 (PROKR2), WDR11, heparin sulfate-6-O-Transferase (HS6T1), chromodomain helicase DNA binding protein 7 (CHD7) and semaphorin 3A (SEMA 3A), additional mutations in "FGF8 synexpression" group e.g., FGF 17, ILRD, DUSP 6, SPRY4 and FLRT3 have been shown to be involved in CHH, mostly KS besides SEMA 7A. Although traditionally division has been based on anosmic/normosnic criteria, further genes found to cause so called nIHH like Gonadotropin releasing hormone receptor (GNRHR). KISS1, TAC3, TACR3 have also been found to be associated with hyposmia on detailed testing on UPSIT and MRI for olfactory structures revealed absent OB. Further detailed examination of transcription factor genes have revealed involvement of HESX1, TSHZ1, AXL, SOX10 with a strong overlap of in transcription factors in development of septooptic dysplasia (SOD), combined pituitary hormone deficiency (CHPD) and KS. Treatment with rFSH/-hCG gives almost similar results to pulsatile GnRH therapy and should be based on cost factor, availability and in occasional cases specific treatment like kisspeptin therapy. Conclusions: Contrary to the traditional thinking, one shoud reconsider classifying cases of IHH simply on basis of anosmia/normosmia. Deafness calls for looking for mutations in Sox 10/CHD7/ILRD7 considering 38% associ-Open Access K. K. Kulvinder et al. 51 ation of former. Therapy should be individualized based on availability of pulsatile GnRH, cost factor and in recalcitrant cases kp therapy may be of use with kp mutations and NKB mutations.

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Kisspeptins in human reproduction—future therapeutic potential

Cited by 8 publications

References 134 publications

An Update on Aetiopathology, Various Genetic Causes and Management of Delayed Puberty-A Minireview

An Update on Aetiopathology, Various Genetic Causes and Management of Delayed Puberty-A Minireview

Has Kisspeptin found a place to be a biomarker in the differentiation of viability of early pregnancy-a short commentary

Idiopathic Hypogonadotropic Hypogonadism— An Update on the Aetiopathogenesis, Management of IHH in Both Males and Females—An Exhaustive Review

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