Myostatin (MSTN) lacking could lead to enhanced muscle growth and lipid metabolism disorder in animals. Plenty of researches have been performed to warrant a better understanding of the mechanisms underlying the enhanced muscle growth; however, mechanisms for lipid metabolic changes are poorly understood. In this study, MSTN-depletion loaches Misgurnus anguillicaudatus (MU for short) were firstly generated by CRISPR/Cas9 technique. Based on histological observation, we found that skeletal muscle fat accumulation in MU sharply reduced compared with wild-type loaches (WT for short). To further investigate the fat change, muscle lipidomic analysis was performed. There were no significant differences in three membrane phospholipid contents between WT and MU. The contents of six other major lipid species in MU muscles were all significantly lower than those in WT muscles, indicating that MSTN deficiency could obviously decrease muscle lipid production in the loach. Meanwhile, it was also supported by results of three lipogenesis-related genes’ expressions. And then combined with muscle ATP determination and gene expression profiles of the five mitochondrial respiration chain complexes, we speculated that MSTN lacking may cause the weak of mitochondrial respiration functions in the loach muscles, leading to ATP synthesis decreasing and finally reducing the production of lipids.

中文翻译：

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通过抑制线粒体呼吸，ATP合成效率低下，导致泥MS Misgurnus anguillicaudatus缺少MSTN的肌肉中脂质减少。

缺乏Myostatin（MSTN）可能导致动物肌肉生长增强和脂质代谢紊乱。已经进行了大量的研究以保证更好地理解增强肌肉生长的机制。但是，对于脂质代谢变化的机制了解甚少。在这项研究中，MSTN耗竭泥Mi Misgurnus anguillicaudatus（MU）最早是通过CRISPR / Cas9技术产生的。根据组织学观察，我们发现与野生型泥（（简称WT）相比，MU中的骨骼肌脂肪积聚急剧减少。为了进一步研究脂肪变化，进行了肌肉脂质组分析。WT和MU之间的三种膜磷脂含量没有显着差异。MU肌肉中其他六种主要脂质种类的含量均显着低于WT肌肉，表明MSTN缺乏可明显降低泥lo中的肌肉脂质产生。同时，这也得到了三个与脂肪生成相关的基因表达的结果的支持。然后结合肌肉ATP测定和五种线粒体呼吸链复合物的基因表达谱，