Researchers found that a peptide called kisspeptin‑10 can change hormone production and how sperm stick to support cells in frog testes, but giving it to live frogs didn’t make sperm get released. The work is basic science in amphibians and doesn’t give clear guidance for human use.

Kisspeptin (Kp) system has a recognized role in the control of gonadotropic axis, at multiple levels. Recently, a major focus of research has been to assess any direct activity of this system on testis physiology. Using the amphibian anuran, <i>Pelophylax esculentus</i>, as animal model, we demonstrate - for the first time in non-mammalian vertebrate - that testis expresses both Kiss-1 and Gpr54 proteins during the annual sexual cycle and that <i>ex vivo</i> 17B-estradiol (E₂, 10^-6&#x2009;M) increases both proteins over control group. Since the interstitium is the main site of localization of both ligand and receptor, its possible involvement in the regulation of steroidogenesis has been evaluated by <i>ex vivo</i> treatment of testis pieces with increasing doses of Kp-10 (10^-9-10^-6&#x2009;M). Treatments have been carried out in February - when a new wave of spermatogenesis occurs - and affect the expression of key enzymes of steroidogenesis inducing opposite effects on testosterone and estradiol intratesticular levels. Morphological analysis of Kp-treated testes reveals higher number of tubules with spermatozoa detached from Sertoli cells than control group and the expression of connexin 43, the main junctional protein in testis, is deeply affected by the treatment. In spite of the effects on spermatozoa observed <i>ex vivo</i>, <i>in vivo</i> administration of Kp-10 has been unable to induce sperm release in cloacal fluid. In conclusion, we demonstrate Kp-10 effects on steroidogenesis with possible involvement in the balance between testosterone and estradiol levels, and report new Kp-10 activities on spermatozoa-Sertoli cell interaction.