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mtch2功能丧失会损害斑马鱼幼体肝脏、肠道和内脏脂肪细胞的早期发育。

Loss of mtch2 function impairs early development of liver, intestine and visceral adipocytes in zebrafish larvae.

作者信息

Landgraf Kathrin, Strobach Ariane, Kiess Wieland, Körner Antje

机构信息

Center for Pediatric Research Leipzig (CPL), University Hospital for Children and Adolescents, University of Leipzig, Germany.

Medical Center AdiposityDiseases (IFB), University of Leipzig, Germany.

出版信息

FEBS Lett. 2016 Sep;590(17):2852-61. doi: 10.1002/1873-3468.12330. Epub 2016 Aug 9.

DOI:10.1002/1873-3468.12330
PMID:27468124
Abstract

The mitochondrial carrier homologue 2 (MTCH2) has been shown to be essential for embryogenesis in mice, and variants in the MTCH2 locus have been linked to obesity in humans. Here, we investigated the importance of mtch2 for embryogenesis and adipocyte formation in zebrafish in vivo. We show that mtch2 is conserved in zebrafish and broadly expressed during embryogenesis. Knock-down of mtch2 results in impaired development of liver and intestine, and is associated with a reduced number of adipocytes and impaired postembryonic growth. The findings indicate an essential role for mtch2 during organ development and adipogenesis in vivo.

摘要

线粒体载体同源物2(MTCH2)已被证明对小鼠胚胎发育至关重要,并且MTCH2基因座中的变异与人类肥胖有关。在此,我们在体内研究了mtch2对斑马鱼胚胎发育和脂肪细胞形成的重要性。我们发现mtch2在斑马鱼中保守,并且在胚胎发育过程中广泛表达。敲低mtch2会导致肝脏和肠道发育受损,并与脂肪细胞数量减少和胚后生长受损有关。这些发现表明mtch2在体内器官发育和脂肪生成过程中起着重要作用。

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FEBS Lett. 2016 Sep;590(17):2852-61. doi: 10.1002/1873-3468.12330. Epub 2016 Aug 9.
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