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Kisspeptin () and kisspeptin 1 receptor () are vital in regulating various functions across many species, primarily those relating to reproduction. The kisspeptin system has recently attracted clinical interest as a potential therapeutic treatment for patients with hypoactive sexual desire disorder. This study maps the distribution of and mRNA in the Syrian hamster forebrain using dual-labeled RNAscope. In our study, the distributions of kisspeptin and its receptor were mapped across adult males and females on day 1 or day 2 of their estrous cycle. Conditioned place preference was used to observe the potential effect of kisspeptin on sexual reward in female hamsters. The expression of kisspeptin was greater in females than males, with the estrous cycle having no effect on expression. A comparison of these findings to those in other species revealed that the expression in Syrian hamsters was similar to that reported for other species, demonstrating the conservation of expression. Kisspeptin did not influence sexual reward in females, nor did it affect measures of their primary sexual behavior. These findings provide additional insights into the expression and function of kisspeptin across novel species and add to ongoing research in understanding how kisspeptin may influence sexual desire in animals, including humans.
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http://dx.doi.org/10.3390/cells14130992 | DOI Listing |
Reprod Domest Anim
September 2025
Department of Teaching Veterinary Clinical Complex, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, Punjab, India.
The present study was undertaken to assess the effect of kisspeptin supplementation (0.0, 5.0, 10.
View Article and Find Full Text PDFJ Biomol Struct Dyn
September 2025
TREE Lab, Department of Biomedical and Life Sciences, School of Science, Navrachana University, Vadodara, India.
Metastasis is a key hallmark of cancer aggressiveness, particularly in triple-negative breast cancer (TNBC), which lacks effective targeted therapies. Kisspeptin-1 (KISS1), a known metastasis suppressor is emerging as a potential therapeutic modulator. This study investigates the structural and regulatory interactions between and key transcription factors (TFs) involved in metastasis: SP1, CDX2, FLI1, GATA2, NMYC, and HDAC2.
View Article and Find Full Text PDFCardiovasc Endocrinol Metab
September 2025
Biochemistry Department, Azerbaijan Medical University, Baku, Azerbaijan.
Central precocious puberty (CPP) results from premature reactivation of the hypothalamic-pituitary-gonadal axis and is increasingly recognized as a systemic condition linked to cardiometabolic health. Genetic mutations, particularly in imprinted genes such as and , are major monogenic causes of familial CPP, while rare activating variants in and highlight the pivotal role of kisspeptin signaling. Neuropeptides, including kisspeptin and neurokinin B, are central to pubertal regulation.
View Article and Find Full Text PDFMolecules
August 2025
Reproductive Physiology Laboratory-UIBR, Facultad de Estudios Superiores Zaragoza, Universidad Nacional Autónoma de México, Mexico City 09230, Mexico.
Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder characterized by a clinical and/or biochemical hyperandrogenism. In addition, PCOS is also associated with the presence of ovarian cysts, anovulation, and menstrual abnormalities such as oligomenorrhea or amenorrhea. The aetiology of the syndrome is multifactorial and heterogeneous due to the interaction of genetic, hormonal, metabolic, and environmental factors, as well as the different phenotypes and responses to treatments exhibited by the patients.
View Article and Find Full Text PDFCells
August 2025
Department of Medicine, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ 08901, USA.
The peptide hormone kisspeptin, signaling via its receptor, KISS1R, decreases hepatic steatosis and protects against metabolic dysfunction-associated steatotic liver disease (MASLD). Enhanced de novo lipogenesis (DNL) contributes to MASLD. Here, we investigated whether kisspeptin treatment in obese, diabetic mice directly attenuates DNL.
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