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Regulation of glucose-stimulated insulin secretion by ATPase Inhibitory Factor 1 (IF1)
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SYSNO ASEP 0490334 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Regulation of glucose-stimulated insulin secretion by ATPase Inhibitory Factor 1 (IF1) Author(s) Kahancová, Anežka (FGU-C)
Sklenář, Filip (FGU-C) RID, ORCID
Ježek, Petr (FGU-C) RID, ORCID
Dlasková, Andrea (FGU-C) RID, ORCIDSource Title FEBS Letters. - : Wiley - ISSN 0014-5793
Roč. 592, č. 6 (2018), s. 999-1009Number of pages 11 s. Language eng - English Country GB - United Kingdom Keywords ATP synthase ; diabetes ; IF1 ; INS-1E cells ; insulin secretion ; beta-cells Subject RIV CE - Biochemistry OECD category Biochemistry and molecular biology R&D Projects LM2015062 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) GJ15-02022Y GA ČR - Czech Science Foundation (CSF) Institutional support FGU-C - RVO:67985823 UT WOS 000428400000014 EID SCOPUS 85042323102 DOI 10.1002/1873-3468.12991 Annotation ATPase Inhibitory factor 1 (IF1) is an endogenous regulator of mitochondrial ATP synthase, which is involved in cellular metabolism. Although great progress has been made, biological roles of IF1 and molecular mechanisms of its action are still to be elucidated. Here, we show that IF1 is present in pancreatic beta-cells, bound to the ATP synthase also under normal physiological conditions. IF1 silencing in model pancreatic beta-cells (INS-1E) increases insulin secretion over a range of glucose concentrations. The left-shifted dose-response curve reveals excessive insulin secretion even under low glucose, corresponding to fasting conditions. A parallel increase in cellular respiration and ATP levels is observed. To conclude, our results indicate that IF1 is a negative regulator of insulin secretion involved in pancreatic beta-cell glucose sensing. Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2019
Number of the records: 1