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肌肉生长抑制素b的缺失促进斑马鱼的体细胞生长和脂质代谢。

Depletion of Myostatin b Promotes Somatic Growth and Lipid Metabolism in Zebrafish.

作者信息

Gao Yanping, Dai Ziru, Shi Chuang, Zhai Gang, Jin Xia, He Jiangyan, Lou Qiyong, Yin Zhan

机构信息

Key Laboratory of Aquatic Biodiversity and Conservation, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China

University of Chinese Academy of Sciences, Beijing, China.

出版信息

Front Endocrinol (Lausanne). 2016 Jul 4;7:88. doi: 10.3389/fendo.2016.00088. eCollection 2016.

Abstract

Myostatin (MSTN) is a negative regulator of myogenesis in vertebrates. Depletion of mstn resulted in elevated muscle growth in several animal species. However, the report on the complete ablation of mstn in teleost fish has not yet become available. In this study, two independent mstnb-deficient mutant lines in zebrafish were generated with the TALENs technique. In the mstnb-deficient zebrafish, enhanced muscle growth with muscle fiber hyperplasia was achieved. Beginning at the adult stage (80 days postfertilization), the mstnb-deficient zebrafish exhibited increased circumferences and body weights compared with the wild-type sibling control fish. Although the overall total lipid/body weight ratios remained similar between the mstnb-deficient zebrafish and the control fish, the distribution of lipids was altered. The size of the visceral adipose tissues became smaller while more lipids accumulated in skeletal muscle in the mstnb-deficient zebrafish than in the wild-type control fish. Based on the transcriptional expression profiles, our results revealed that lipid metabolism, including lipolysis and lipogenesis processes, was highly activated in the mstnb-deficient zebrafish, which indicated the transition of energy metabolism from protein-dependent to lipid-dependent in mstnb-deficient zebrafish. Our mstnb-deficient model could be valuable in understanding not only the growth trait regulation in teleosts but also the mechanisms of teleost energy metabolism.

摘要

肌肉生长抑制素(MSTN)是脊椎动物肌肉生成的负调控因子。在几种动物物种中,mstn缺失导致肌肉生长增加。然而,关于硬骨鱼中mstn完全缺失的报道尚未出现。在本研究中,利用转录激活样效应因子核酸酶(TALENs)技术构建了两个独立的斑马鱼mstnb基因缺失突变系。在mstnb基因缺失的斑马鱼中,实现了肌肉纤维增生从而促进肌肉生长。从成年期(受精后80天)开始,与野生型同胞对照鱼相比,mstnb基因缺失的斑马鱼周长和体重增加。虽然mstnb基因缺失的斑马鱼与对照鱼的总脂质/体重比总体相似,但脂质分布发生了改变。与野生型对照鱼相比,mstnb基因缺失的斑马鱼内脏脂肪组织变小,而骨骼肌中积累了更多脂质。基于转录表达谱,我们的结果显示,脂质代谢,包括脂解和脂肪生成过程,在mstnb基因缺失的斑马鱼中高度激活,这表明mstnb基因缺失的斑马鱼能量代谢从蛋白质依赖型向脂质依赖型转变。我们构建的mstnb基因缺失模型不仅对理解硬骨鱼的生长性状调控,而且对理解硬骨鱼能量代谢机制都具有重要价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09bb/4930940/49d71f449d01/fendo-07-00088-g001.jpg

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