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Kisspeptin-10

KP-10, Metastin (45-54), Kisspeptin-10 (human), KiSS-1

Quick Stats
Studies 877
Trials 47
Score 2
2021 pubmed

MINI REVIEW: Role of Kisspeptin-GPR54 system in regulation of reproductive functions in human and other mammals.

Ilahi. Ikram I; Haq. Taqweem Ul TU

Key Findings

  • Kisspeptin binds GPR54 to regulate puberty and reproductive hormone pathways
  • Loss‑of‑function mutations in KISS1 or KISS1R cause hypogonadotropic hypogonadism, while gain‑of‑function mutations lead to central precocious puberty
  • Elevated blood kisspeptin levels can serve as a biomarker for diagnosing central precocious puberty

Practical Outcomes

  • While the paper doesn’t give dosing or supplement advice, it highlights kisspeptin’s central role in hormone regulation, suggesting that any self‑experimentation aimed at modulating reproductive hormones should consider the kisspeptin‑GPR54 pathway. Measuring blood kisspeptin could be useful for tracking hormonal status, but more research is needed before practical protocols can be recommended.

Summary

Kisspeptin is a small protein that talks to a receptor called GPR54 and helps control the whole reproductive system, from brain signals that start puberty to hormone release and even sperm activity. Changes in the kisspeptin gene or its receptor can cause delayed puberty or early puberty, and higher kisspeptin levels in blood can signal early puberty. The study mainly explains how this system works and why it matters for reproductive health.

Abstract

Kisspeptin is a 54- amino acid peptide that acts as a ligand of a receptor called GPR54 which is basically a transmembrane receptor that spins seven times across the cell membrane and coupled with G-protein. Kisspeptin regulates the development of reproductive functions and the onset of puberty in human and other mammals by acting at the brain, hypothalamus, pituitary and gonad levels of reproductive axis. Kisspeptin is also involved in regulation of trophoblastic invasion during pregnancy, ovulation, and sperm hyperactivation. Inactivating mutations in human kisspeptin gene (KISS1) cause idiopathic hypogonadotropic hypogonadism. Some mutations in human kisspeptin receptor gene (KISS1R) make the receptor inactive which result in idiopathic hypogonadotropic hypogonadism. Some mutations in human KISS1R gene make the receptor prematurely activated and result in the development of central precocious puberty. Central precocious puberty is also caused by some mutations in human KISS1 gene that make the kisspeptin resistant to degradation. This leads to an increased basal kisspeptin level and subsequently the development of central precocious puberty. Higher kisspeptin level has been detected in the serum and plasma of central precocious puberty patients, which suggest that serum or plasma kisspeptin level can be used as a marker for diagnosis of central precocious puberty.

Study Information

Provider

pubmed

Year

2021