Leptin increases L-type Ca²⁺ channel expression and GnRH-stimulated LH release in LβT2 gonadotropes

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• 作者：José ; E. Avelino-Cruz ; Amira Flores ; Jorge Cebada ; Pamela L. Mellon ; Ricardo Felix ; Eduardo Monjaraz
• 关键词：Ca²⁺ channels ; Lβ ; T2 cells ; Leptin ; Patch-cl Pituitary ; Gonadotropes
• 刊名：Molecular and Cellular Endocrinology
• 出版年：2009
• 出版时间：27 January 2009
• 年：2009
• 卷：298
• 期：1-2
• 页码：57-65
• 全文大小：1010 K

文摘

Leptin, a mediator of long-term regulation of energy balance, has been implicated in the release of adenohypophyseal gonadotropins by regulating gonadotropin-releasing hormone (GnRH) secretion from the hypothalamus. However, a direct effect of leptin on hormone release from gonadotropes remains virtually unexplored. In the current report, we assessed the long-term (48 h) actions of leptin on voltage-gated channel activity and luteinizing hormone (LH) production in mouse pituitary gonadotrope LβT2 cells. Electrophysiological recordings showed that leptin treatment significantly increased whole-cell patch-clamp Ba²⁺ current through L-type Ca²⁺ channels. Quantitative RT-PCR analysis revealed increased levels of L-type (α_1D) Ca²⁺ channel mRNA. Likewise, radioimmunoassays using specific antibodies provided evidence that leptin alone had no effect on LH release but did enhance GnRH-induced secretion of the hormone. Leptin had no apparent effects on LH gene transcription in absence of GnRH, as measured by transient transfection assays using a LH promoter-reporter gene and real-time RT-PCR. These observations suggest that leptin might affect LH release by acting directly on the gonadotropes, favoring hormone production by enhancing responsiveness to GnRH as a result of increased Ca²⁺ channel expression.