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Sci Rep. 2017 Aug 8;7(1):7606. doi: 10.1038/s41598-017-08081-z.

Deficiency of COX7RP, a mitochondrial supercomplex assembly promoting factor, lowers blood glucose level in mice.

Author information

1
Division of Gene Regulation and Signal Transduction, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan.
2
Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
3
Division of Gene Regulation and Signal Transduction, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan. sinoue@tmig.or.jp.
4
Department of Functional Biogerontology, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan. sinoue@tmig.or.jp.

Abstract

Mitochondria are essential organelles to efficiently produce ATP by ATP-synthase, which uses a proton-gradient generated by respiratory chain complexes. We previously demonstrated that COX7RP/COX7A2L/SCAF1 is a key molecule that promotes respiratory supercomplex assembly and regulates energy generation. The contribution of COX7RP to metabolic homeostasis, however, remains to be clarified. In the present study, we showed a metabolic phenotype of Cox7rp knockout (Cox7rpKO) mice, which exhibit lower blood glucose levels after insulin or pyruvate injection. Notably, ATP synthesis rate was reduced in Cox7rpKO mice liver, in accordance with decreased percentages of complex III subunit RISP and complex IV subunit COX1 involved in I + III + IV supercomplex fraction. The present findings suggest that COX7RP-mediated mitochondrial respiration plays crucial roles in the regulation of glucose homeostasis and its impairment will lead to the pathophysiology of metabolic states.

PMID:
28790391
PMCID:
PMC5548899
DOI:
10.1038/s41598-017-08081-z
[Indexed for MEDLINE]
Free PMC Article

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