外源性leptin对离体黄颡鱼卵巢滤泡细胞脂代谢的影响
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摘要
瘦素(leptin)是主要由脂肪细胞分泌的激素类细胞因子,同机体的能量代谢密切相关。本实验探究了黄颡鱼卵巢滤泡细胞的分离程序,并通过设置不同的处理组(control、0.1%DMSO、500 ng/ml leptin、500 ng/ml leptin+100μM wortmannin、500 ng/ml leptin+50n M AG490),研究离体条件下外源性leptin对黄颡鱼原代培养卵巢滤泡细胞脂代谢影响及其潜在通路的模型。实验结果表明:leptin的添加显著性降低了TG含量和FAS,G6PD and 6PGD,SREBP-1 and PPARγ的活性和基因表达量,并导致CPT I,PPARαand ACCa的活性和基因表达量升高;添加抑制剂后,能够显著性影响leptin对几种脂代谢相关酶的活性和基因表达量,而减缓了leptin的作用效果。从而说明,leptin可能通过JAK-STAT和IRS-PI3K信号通路来调控脂类代谢。
The present study was conducted to determine the effect of leptin on lipid metabolism in ovarian follicle cells of yellow catfish Pelteobagrus fulvidraco. For that purpose, primary ovarian follicle cells were isolated from yellow catfish, cultured and subjected to different treatments(control, 0.1% DMSO, 500 ng/ml leptin, 500 ng/ml leptin + 100 l M wortmannin, 500ng/ml leptin + 50 n M AG490, respectively) for 48 h. Recombinant human leptin(rt-h LEP)incubation significantly reduced intracellular TG content, activities and mRNA levels of FAS,G6 PD and 6PGD, SREBP-1 and PPARc, but enhanced activity and mRNA level of CPT I, PPARa and ACCa. Specific inhibitors AG490 and wortmannin of JAK–STAT and IRS–PI3K signaling pathways prevented leptin-induced changes, indicating that JAK–STAT and IRS–PI3K signaling pathways were involved in the process of leptin-induced changes of lipid metabolism. Based on these observationsabove, for the first time, our study indicated that leptin reduced lipid deposition by activating lipolysisand suppressing lipogenesis in ovarian follicles of yellow catfish.
引文

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