Open AccessGonadotrophin‐releasing hormone‐I and‐II stimulate steroidogenesis in prepubertal murine Leydig cells in vitro
Author(s) -
Lin YungMing,
Liu MingYie,
Poon SongLing,
Leu SewFen,
Huang BuMiin
Publication year - 2008
Publication title -
asian journal of andrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 74
eISSN - 1745-7262
pISSN - 1008-682X
DOI - 10.1111/j.1745-7262.2008.00434.x
Subject(s) - leydig cell , cholesterol side chain cleavage enzyme , medicine , endocrinology , steroidogenic acute regulatory protein , testosterone (patch) , gonadotropin releasing hormone , hormone , in vitro , chemistry , enzyme , biology , messenger rna , cytochrome p450 , luteinizing hormone , metabolism , gene , biochemistry
Aim: To study the effect and mechanism of gonadotrophin‐releasing hormone (GnRH) on murine Leydig cell steroidogenesis. Methods: Purified murine Leydig cells were treated with GnRH‐I and‐II agonists, and testosterone production and steroidogenic enzyme expressions were determined. Results: GnRH‐I and‐II agonists significantly stimulated murine Leydig cell steroidogenesis 60%–80% in a dose‐and time‐dependent manner ( P < 0.05). The mRNA expressions of steroidogenic acute regulatory (StAR) protein, P450scc, 3β‐hydroxysteroid dehydrogenase (HSD), but not 17α‐hydroxylase or 17β‐HSD, were significantly stimulated by both GnRH agonists with a 1.5‐to 3‐fold increase ( P < 0.05). However, only 3β‐HSD protein expression was induced by both GnRH agonists, with a 1.6‐to 2‐fold increase ( P < 0.05). Conclusion: GnRH directly stimulated murine Leydig cell steroidogenesis by activating 3β‐HSD enzyme expression.