Brandebourg Terry D, Bown Jenna L, Ben-Jonathan Nira
Department of Cell and Cancer Biology, University of Cincinnati College of Medicine, 3125 Eden Avenue, Cincinnati, OH 45267-0521, USA.
Biochem Biophys Res Commun. 2007 Jun 1;357(2):408-13. doi: 10.1016/j.bbrc.2007.03.168. Epub 2007 Apr 5.
Prolactin (PRL) is recognized as a metabolic regulator during lactation, but little information exists on its actions in male adipose tissue. We examined whether PRL affects the expression of its receptors (PRLR), lipolysis, and adipokine secretion in male rats. Both long and short PRLR isoforms were induced 40-50-fold during differentiation of epididymal preadipocytes, with a 10-fold higher expression of the long isoform. PRL upregulated both isoforms before and after differentiation. PRL suppressed lipolysis in epididymal explants and mature adipocytes in a dose- and time-dependent manner, which was reversed by a Jak2 inhibitor. PRL also inhibited leptin, but not adiponectin, release. We conclude that PRL inhibits lipolysis and leptin release by acting directly on adipocytes via interaction with either of its receptors and activation of a Jak2-dependent signaling pathway(s). This is the first demonstration of substantial effects of PRL on male adipocytes.
催乳素(PRL)在哺乳期被认为是一种代谢调节因子,但关于其在雄性脂肪组织中的作用的信息却很少。我们研究了PRL是否会影响雄性大鼠中其受体(PRLR)的表达、脂肪分解以及脂肪因子的分泌。在附睾前脂肪细胞分化过程中,长型和短型PRLR异构体均被诱导40 - 50倍,长型异构体的表达高10倍。PRL在分化前后均上调了这两种异构体。PRL以剂量和时间依赖性方式抑制附睾外植体和成熟脂肪细胞中的脂肪分解,这一作用被Jak2抑制剂逆转。PRL还抑制瘦素释放,但不抑制脂联素释放。我们得出结论,PRL通过与其任一受体相互作用并激活Jak2依赖性信号通路,直接作用于脂肪细胞,从而抑制脂肪分解和瘦素释放。这是PRL对雄性脂肪细胞产生显著影响的首次证明。