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Erschienen in: Endocrine 1/2014

01.02.2014 | Original Article

The effect of chronic kisspeptin administration on seminal fructose levels in male mice

verfasst von: Faiqah Ramzan, Muhammad Ayaz Khan, Muhammad Haris Ramzan

Erschienen in: Endocrine | Ausgabe 1/2014

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Abstract

The discovery that kisspeptin was critical for normal fertility in all mammalian species including humans, ushered in a new chapter in our understanding of the control of GnRH secretion. Kisspeptin, the product of the KISS1 gene, plays an essential role in the regulation of spermatogenesis acting primarily at the hypothalamic level of the gonadotropic axis. Among the many identified substances in human semen, fructose is becoming increasingly significant. Fructose is synthesized and secreted by the seminal vesicles. Its synthesis is regulated by androgens and it is correlated directly with the levels of testosterone. Dose dependent degeneration of seminal vesicle has been described following intraperitoneal kisspeptin treatment; however, effects of kisspeptin administration on the levels of seminal fructose remain elusive till date. The present study, therefore, addresses the effects of 12-day administration of kisspeptin on seminal fructose levels in male mice. Kisspeptin-10 was administered intraperitoneally at different dosage concentrations (1 μg, 1 ng, and 10 ρg) to adult male mice, twice daily for 12 days. Seminal fructose levels were studied photometrically after 12 days of treatment. At the end of the treatment, seminal fructose levels decreased significantly after all tested doses. Chronic intermittent kisspeptin-10 administration negatively regulates seminal fructose levels in adult male mice.
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Metadaten
Titel
The effect of chronic kisspeptin administration on seminal fructose levels in male mice
verfasst von
Faiqah Ramzan
Muhammad Ayaz Khan
Muhammad Haris Ramzan
Publikationsdatum
01.02.2014
Verlag
Springer US
Erschienen in
Endocrine / Ausgabe 1/2014
Print ISSN: 1355-008X
Elektronische ISSN: 1559-0100
DOI
https://doi.org/10.1007/s12020-013-0016-x

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