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Inhibition of GSK3β Reduces Ectopic Lipid Accumulation and Induces Autophagy by The AMPK Pathway in Goat Muscle Satellite Cells

机译:GSK3β的抑制作用降低了山羊肌肉卫星细胞中AMPK途径的异位脂质蓄积并诱导自噬

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摘要

Ectopic lipid accumulation in muscle is important not only for obesity and myopathy treatment, but also for meat quality improvement in farm animals. However, the molecular mechanisms involved in lipid metabolism in muscle satellite cells are still elusive. In this study, SB216763 reduced GSK3β activation by increasing the level of pGSK3β (Ser9) and decreasing the level of total GSK3β protein. GSK3β inhibition decreased lipid accumulation and downregulated the expression level of lipogenesis-related genes in the adipogenic differentiation of goat muscle satellite cells. Furthermore, SB216763 treatment increased the levels of pAMPKα (T172) and pACC (Ser79). Further, we found that GSK3β inhibition promoted levels of LC3B-II and reduced the protein levels of p62 to induce the autophagy in muscle satellite cells. Taken together, our results provide new insight into a critical function for GSK3β: modulating lipid accumulation in goat muscle satellite cells through activating the AMPK pathway.
机译:肌肉中异位脂质的积累不仅对肥胖和肌病治疗很重要,而且对改善农场动物的肉质也很重要。但是,参与肌肉卫星细胞脂质代谢的分子机制仍然难以捉摸。在这项研究中,SB216763通过增加pGSK3β(Ser9)的水平和降低总GSK3β蛋白的水平来降低GSK3β的激活。 GSK3β抑制作用降低了山羊肌肉卫星细胞成脂分化中脂质的积累,并下调了脂肪形成相关基因的表达水平。此外,SB216763处理可提高pAMPKα(T172)和pACC(Ser79)的水平。此外,我们发现,GSK3β抑制可促进LC3B-II的水平并降低p62的蛋白水平,从而诱导肌肉卫星细胞中的自噬。综上所述,我们的结果为GSK3β的关键功能提供了新的见解:通过激活AMPK途径调节山羊肌肉卫星细胞中脂质的积累。

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