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Kisspeptin-10

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

Quick Stats
Studies 877
Trials 47
Score 2
2011 pubmed 97 citations

Characterization of the kisspeptin system in human spermatozoa.

Pinto. F M FM; Cejudo-Román. A A; Ravina. C G CG; Fernández-Sánchez. M M; Martín-Lozano. D D; Illanes. M M; Tena-Sempere. M M; Candenas. M L ML

Key Findings

  • Kisspeptin and its receptor KISS1R are localized in the head, neck, and midpiece of human sperm
  • Kisspeptin exposure causes a slow, progressive increase in intracellular Ca2+ in sperm
  • Kisspeptin produces a biphasic effect on sperm progressive motility and induces transient hyperactivation, effects blocked by a KISS1R antagonist
  • Kisspeptin does not induce the acrosome reaction in human sperm

Practical Outcomes

  • At this stage kisspeptin isn’t ready for any DIY fertility or performance protocol – the study was done in vitro and didn’t define safe doses or delivery methods. It does suggest that targeting the kisspeptin pathway could one day influence sperm motility, but more research is needed before any practical supplementation or treatment can be recommended.

Summary

Researchers found that the hormone kisspeptin and its receptor are actually present in human sperm cells. When sperm are exposed to kisspeptin in the lab, calcium levels rise slowly, and sperm movement changes in a two‑phase pattern – first it speeds up, then it slows down, and there’s a brief boost in a vigorous swimming style called hyperactivation. However, kisspein doesn’t trigger the sperm’s acrosome reaction, which is needed for fertilization, and blocking its receptor stops these effects.

Abstract

Kisspeptin, the product of the KISS1 gene, plays an essential role in the regulation of spermatogenesis acting primarily at the hypothalamic level of the gonadotropic axis. However, the presence of kisspeptin and its canonical receptor, KISS1R, in spermatozoa has not been explored nor the direct effects of kisspeptin on sperm function have been studied so far. In the present study, we analysed the expression of kisspeptin and its receptor in sperm cells by western blot and immunocytochemistry assays and evaluated the effects of exposure to kisspeptin on sperm intracellular Ca(2+) concentration, [Ca(2+)]i, sperm motility, sperm hyperactivation and the acrosome reaction. Changes in [Ca(2+)]i were monitored using Fura-2, sperm kinematic parameters were measured using computer-assisted sperm analysis (CASA), and the acrosome reaction was measured using fluorescein isothiocyanate-coupled Pisum sativum agglutinin lectin (FITC-PSA method). We found that kisspeptin and its receptor are present in sperm cells, where both are mainly localized in the sperm head, around the neck and in the flagellum midpiece. Exposure to kisspeptin caused a slow, progressive increase in [Ca(2+)]i, which reached a plateau about 3-6 min after kisspeptin exposure. In addition, kisspeptin modulated sperm progressive motility causing a biphasic (stimulatory and inhibitory) response and also induced transient sperm hyperactivation. The effects of kisspeptin on sperm motility and hyperactivation were inhibited by the antagonist of KISS1R, peptide 234. Kisspeptin did not induce the acrosome reaction in human spermatozoa. These data show for the first time that kisspeptin and its receptor are present in human spermatozoa and modulate key parameters of sperm function. This may represent an additional mechanism for their crucial function in the control of male fertility.

Study Information

Provider

pubmed

Year

2011

Date

2011-06-09T00:00:00.000Z

DOI

10.1111/j.1365-2605.2011.01177.x

Citations

97

References

43