IntroductionKisspeptins, the peptide products of the KiSS-1 gene, bind to the G protein-coupled receptor 54 (GPR54), a critical regulator of GnRH secretion. The N-terminally truncated peptide metastin 45-54 exhibits 10-fold higher receptorbinding affinity than full-length metastin; it also shows agonistic KISS-1R activity (1).Kisspeptins are known to play a role in puberty, cancer metastasis, and vasoconstriction (2,3-7). They are synthesized in the arcuate and anteroventral periventricular hypothalamic neurons and in the perioptic area (8). Kisspeptin expression is variable according to sex in rats; its expression is more marked in female animals (9). Its known derivatives are kisspeptin-10, kisspeptin-13, kisspeptin-14, and kisspeptin-54 (10-12). All kisspeptins seem to have the same interactions under in vitro conditions. Kiss-10 is well characterized in mammals, in which it is found in large concentrations (10,11). It has been suggested, however, that Kiss-54 is the most effective form (12). Kisspeptin has been reported to also be synthesized in the testes, ovaries, pancreas, gut, liver, lung, muscle tissue, kidney, nervous system, and most densely in the placenta (13,14). As for its receptor, G protein-coupled receptor-54 (GPR54) is mostly expressed in the hypophysis, placenta, and pancreas (10,15,16). Kisspeptins are highly potent neuropeptides that stimulate the secretion of LH and FSH from the hypophysis, an effect exerted through the release of GnRH (7,17). While this pathway has been satisfactorily defined in several mammal species, the molecular and cellular events at the proencephalic origin of this process are incompletely elucidated. In recent years, studies have indicated that kisspeptin plays a role in the transition to puberty (18,19). Kiss-1 knockout mice showed hypogonadism and low Background/aim: To study the effect of kisspeptin, a gonadotropin release stimulator, on the testicular tissue of the rat.Materials and methods: Four groups were formed as follows: control, Kiss-10 50 nmol administration for 1 day, Kiss-10 administration for 13 days, and one last group kept for 7 days following Kiss-10 applied for 13 days. Testicular tissues were stained with hematoxylineosin, periodic acid Schiff, Masson trichrome staining, terminal deoxynucleotidyl transferased UTP nick-end labeling, and Ki-67 immune staining. Serum testosterone levels were determined.Results: Serum testosterone level increased following acute application, while it was reduced by chronic treatment. Spermatogenic cells as stained by Ki-67 and TUNEL increased in the treated groups compared to the controls. Following a 7-day rest after treatment, a decrease in testosterone levels and Ki-67-stained cell numbers and an increase in TUNEL-stained cells were observed. Leydig cells showed increased vacuolization in the Kiss-1 group. Leydig cell vacuolization continued in the Kiss (13) group and was reduced in the Kiss (13 + 7) group.
Conclusion:Kiss-10 increased spermatogenic cell proliferation, while testosterone level and proliferation de...