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镁对黄颡鱼肝脏脂肪代谢的影响及其分子机制
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摘要
本实验采用活体饲喂以及离体肝细胞孵育Mg SO4相结合的方法探究镁对黄颡鱼肝脏脂肪代谢的影响及其分子机制。养殖试验表明饲料镁添加缓和了肝脏过度的脂肪沉积,H&E和油红切片进一步确认了这一结果。随着饲料镁含量的增加,6PGD和ME脂肪生成酶的活性降低,而脂肪分解基因ATGL和PPARα的mRNA表达增加。细胞实验表明镁抑制了G6PD,6PGD,ICDH,ME和FAS脂肪生成酶活性,下调了脂肪生成基因G6PD,6PGD,ACCα,FAS,PPARγ,SREBP-1和LXR mRNA水平,但是上调了脂肪分解基因ATGL和PPARαmRNA的表达。使用特异性的信号通路抑制剂或激活剂GW6471(PPARα抑制剂),Troglitazone(PPARγ激活剂),AG490(JAK抑制剂),Compound C(AMPK抑制剂),镁诱导的脂肪代谢变化均被改变,随之降低的肝细胞TG浓度得到恢复。综上所述,镁可能通过JAK-STAT和AMPK信号通路调控脂肪合成和分解代谢,降低了肝脏脂肪沉积。
Two in vivo and in vitro experiments were conducted to explore the effect and molecular mechanisms of magnesium on lipid metabolism for yellow catfish Pelteobagrus fulvidraco. The feeding study showed that dietary magnesium alleviated hepatic excess fat accumulation, as determined by Oil red O and H&E staining. With increasing dietary Mg supplementation, 6PGD and ME lipogenic enzyme activities declined, while mRNA expressions of two lipolytic genes(ATGL and PPARα) increased. For in vitro study, with the specific pathway activators or inhibitors GW6471(PPARα inhibitor), Troglitazone(PPARγ activator), AG490(JAK inhibitor), Compound C(AMPK inhibitor), the Mg SO4-induced down-regulation of G6 PD, 6PGD,ICDH, ME and FAS lipogenic enzyme activities, and lipogenic genes(G6PD, 6PGD, ACCα, FAS,PPARγ, SREBP-1 and LXR) mRNA levels, as well as up-regulation of lipolytic genes(ATGL and PPARα) mRNA levels were altered and, consequently, the reduction of hepatocytes TG concentration were reverted.
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