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In vitro study reveals that GnRH-I and GnRH-II stimulate steroidogenesis in prepubertal murine Leydig cells, highlighting a direct regulatory role for 3beta-hydroxysteroid dehydrogenase.
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, 3beta-hydroxysteroid dehydrogenase (HSD), but not 17alpha-hydroxylase or 17beta-HSD, were significantly stimulated by both GnRH agonists with a 1.5- to 3-fold increase (P < 0.05). However, only 3beta-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 3b-HSD enzyme expression.
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Lin et al. (2008) studied this question.
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