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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 40 citations

The role of sexual steroid hormones in the direct stimulation by Kisspeptin-10 of the secretion of luteinizing hormone, follicle-stimulating hormone and prolactin from bovine anterior pituitary cells.

Ezzat. A Ahmed AA; Saito. H H; Sawada. T T; Yaegashi. T T; Goto. Y Y; Nakajima. Y Y; Jin. J J; Yamashita. T T; Sawai. K K; Hashizume. T T

Key Findings

  • Kisspeptin‑10 raises LH secretion only after estradiol or testosterone exposure, not after progesterone.
  • Kisspeptin‑10 does not change FSH release under any hormone condition.
  • Kisspeptin‑10 increases prolactin release independent of sex‑steroid pretreatment and is less potent than GnRH/TRH.

Practical Outcomes

  • Kisspeptin‑10 isn’t a strong, stand‑alone tool for boosting LH or FSH in humans, especially at the high doses used in the study. Any potential benefit may depend on the presence of estrogen or testosterone, and its overall effect is weaker than standard hormonal signals. Biohackers should view it as a research curiosity rather than a ready‑to‑use supplement for hormone optimization.

Summary

In cow pituitary cells, the short peptide kisspeptin‑10 can boost the release of the male hormone LH, but only when the cells have been exposed to estrogen or testosterone first. It doesn’t affect the release of FSH, and it does raise prolactin levels regardless of hormone pretreatment. However, its effects are weaker than the body’s natural triggers GnRH and TRH, so it’s not a powerful direct stimulator.

Abstract

The aims of the present study were to clarify the effect of Kisspeptin-10 (Kp10) on the secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) from bovine anterior pituitary (AP) cells and evaluate the ability of sex steroids to enhance the sensitivity of gonadotropic and lactotropic cells to Kp10. AP cells prepared from 7-week-old male calves were incubated for 12h with estradiol (E(2); 10(-8)M), progesterone (P(4); 10(-8)M), testosterone (T; 10(-8)M), or vehicle only (control), and then for 2h with Kp10 (10(-6)M). The amounts of LH, FSH and PRL released into the culture medium after the 2-h incubation period were examined. Kp10 significantly stimulated the secretion of LH from the AP cells treated with E(2) and T (P<0.05), but not from the P(4)-treated cells. In contrast, Kp10 had no effect on the secretion of FSH regardless of the steroid treatment. Kp10 significantly stimulated the secretion of PRL (P<0.05), the sexual steroid hormones having no effect. The LH- or FSH-releasing response to gonadotropin-releasing hormone (GnRH; 10(-8)M) and PRL-releasing response to thyrotropin-releasing hormone (TRH; 10(-8)M) were significantly greater than those to Kp10 (P<0.05). The present results suggest that E(2) and T, but not P(4), enhance the sensitivity of gonadotropic cells to the secretion of LH in response to Kp10. However, Kp10 had no stimulatory effect on the secretion of FSH regardless of the effect of sex steroids. Kp10 directly stimulates the secretion of PRL from the pituitary cells, and sex steroids do not enhance the sensitivity of lactotropic cells to Kp10. Furthermore, the LH- and FSH-releasing effect and the PRL-releasing effect of Kp10 are less potent than that of GnRH and TRH, respectively.

Study Information

Provider

pubmed

Year

2010

Date

2010-06-11T00:00:00.000Z

DOI

10.1016/j.anireprosci.2010.06.002

Citations

40

References

41