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Kisspeptin-10

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

Quick Stats
Studies 877
Trials 47
Score 2
2010 pubmed 18 citations

Kisspeptins and the metabolic control of reproduction: physiologic roles and physiopathological implications.

Tena-Sempere. M M

Key Findings

  • Kisspeptin is a key neuropeptide that regulates the gonadotropic (reproductive) axis.
  • Hypothalamic Kiss1 neurons act as a bridge, transmitting metabolic cues such as leptin to reproductive centers via a kisspeptin‑GnRH pathway.
  • The signaling may involve downstream molecules Crtc1 and mTOR, linking energy sensing to hormone release.

Practical Outcomes

  • The main takeaway is that your metabolic health can directly affect fertility through kisspeptin signaling. While this insight could eventually lead to new ways to boost reproductive function or metabolic balance, there are no current dosage guidelines or protocols for biohackers to apply.

Summary

Researchers found that a brain peptide called kisspeptin helps connect the body’s energy status to the hormones that control reproduction. In mice, kisspeptin neurons receive signals like leptin (a fat‑derived hormone) and pass them on to GnRH, the master hormone for fertility, possibly using the Crtc1 and mTOR pathways. This shows a direct link between metabolism and reproductive health, but the work is still early and in animals only.

Abstract

In this presentation, we have provided a succinct state-of-the-art of our knowledge on kisspeptins, the newly identified neuropeptide system with key roles in the control of the gonadotropic axis, in the metabolic regulation of puberty onset and fertility. The experimental evidence revised herein, gathered mostly in rodent models, supports the contention that hypothalamic Kiss1 neurons do operate as a central conduit for conveying metabolic information onto the centers governing reproductive function, through a putative leptin-kisspeptin-GnRH pathway, which is likely to involve Crtc1 and/or mTOR as molecular mediators.

Study Information

Provider

pubmed

Year

2010

Date

2010-04-02T00:00:00.000Z

DOI

10.1016/j.ando.2010.02.018

Citations

18

References

7