Regulation of glucose-stimulated insulin secretion by ATPase Inhibitory Factor 1 (IF1)
Language English Country Great Britain, England Media print-electronic
Document type Letter, Research Support, Non-U.S. Gov't
- Keywords
- ATP synthase, IF1, INS-1E cells, diabetes, insulin secretion, β-cells,
- MeSH
- Insulin-Secreting Cells cytology metabolism MeSH
- Glucose metabolism MeSH
- Insulin metabolism MeSH
- Rats MeSH
- Cell Line, Tumor MeSH
- Rats, Wistar MeSH
- ATPase Inhibitory Protein MeSH
- Proteins metabolism MeSH
- Oxygen Consumption physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Letter MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Glucose MeSH
- Insulin MeSH
- Proteins MeSH
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 β-cells, bound to the ATP synthase also under normal physiological conditions. IF1 silencing in model pancreatic β-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 β-cell glucose sensing.
References provided by Crossref.org
Contribution of Mitochondria to Insulin Secretion by Various Secretagogues
The Pancreatic β-Cell: The Perfect Redox System
Glucose-Induced Expression of DAPIT in Pancreatic β-Cells
Contribution of Oxidative Stress and Impaired Biogenesis of Pancreatic β-Cells to Type 2 Diabetes
Fatty Acid-Stimulated Insulin Secretion vs. Lipotoxicity
