...
首页> 外文期刊>Fish Physiology and Biochemistry >GSK-3 beta participates in the regulation of hepatic lipid deposition in large yellow croaker (Larmichthys crocea)
【24h】

GSK-3 beta participates in the regulation of hepatic lipid deposition in large yellow croaker (Larmichthys crocea)

机译:GSK-3 beta参与大黄鱼(Larmichthys crocea)中肝脏脂质沉积的调节

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

In this study, the participation of glycogen synthase kinase-3 beta (GSK-3 beta) in the lipid deposition was investigated in the liver of large yellow croaker (Larmichthys crocea) by LiCl treatment. It was found that the expression of GSK-3 beta and peroxisome proliferator-activated receptor-gamma (PPAR gamma) was inhibited, but the expression of beta-catenin was induced by LiCl treatment. Furthermore, the gene expression and activity of fatty acid synthetase (FAS) and lipoprotein lipase (LPL) in the liver was inhibited by LiCl treatment. The content of total cholesterol (TC), triglyceride (TG), and non-estesterified fatty acid in the liver, as well as TC, TG, and low-density lipoprotein cholesterol in plasma, was decreased by LiCl treatment. However, high-density lipoprotein cholesterol in plasma was increased, and the number of lipid droplets in the liver was decreased by LiCl treatment. The results indicate that GSK-3 beta/beta-catenin may participate in regulating LPL and FAS through PPAR gamma in the liver of large yellow croaker, which will lead to the inhibition of hepatic lipid deposition.
机译:在这项研究中,通过LiCl处理研究了大黄鱼(Larmichthys crocea)肝脏中糖原合酶激酶3 beta(GSK-3 beta)参与脂质沉积。发现抑制了GSK-3β和过氧化物酶体增殖物激活的受体-γ(PPARγ)的表达,但是通过LiCl处理诱导了β-连环蛋白的表达。此外,LiCl处理可抑制肝脏中脂肪酸合成酶(FAS)和脂蛋白脂肪酶(LPL)的基因表达和活性。 LiCl处理可降低肝脏中总胆固醇(TC),甘油三酸酯(TG)和非酯化脂肪酸的含量,以及血浆中TC,TG和低密度脂蛋白胆固醇的含量。然而,通过LiCl处理,血浆中的高密度脂蛋白胆固醇增加,并且肝脏中的脂质滴的数量减少。结果表明,GSK-3β/β-catenin可能通过大黄鱼肝脏中的PPARγ参与调节LPL和FAS,从而抑制肝脂质沉积。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号