Regulation of glucose-stimulated insulin secretion by ATPase Inhibitory Factor 1 (IF1)

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F18%3A00490334" target="_blank" >RIV/67985823:_____/18:00490334 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1002/1873-3468.12991" target="_blank" >http://dx.doi.org/10.1002/1873-3468.12991</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/1873-3468.12991" target="_blank" >10.1002/1873-3468.12991</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Regulation of glucose-stimulated insulin secretion by ATPase Inhibitory Factor 1 (IF1)

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Regulation of glucose-stimulated insulin secretion by ATPase Inhibitory Factor 1 (IF1)

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10608 - Biochemistry and molecular biology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2018

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

FEBS Letters

ISSN

1873-3468

e-ISSN

—

Svazek periodika

592

Číslo periodika v rámci svazku

6

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

11

Strana od-do

999-1009

Kód UT WoS článku

000428400000014

EID výsledku v databázi Scopus

2-s2.0-85042323102