Abstract

Mitochondria play a key role in insulin secretion by pancreatic beta cells due to their control over the cellular metabolism and namely ATP generation. Previous studies have shown that glucose levels have direct impact on superoxide formation by the mitochondrial respiratory chain. In turn, mitochondrial superoxide has been described to induce remodeling of mitochondrial morphology. In this study we examined mitochondrial superoxide formation under various glucose concentrations in association with mitochondrial morphology. To monitor in situ surplus superoxide O2●– released to the mitochondrial matrix (Jm) we employed confocal fluorescence microscopy time scanning of MitoSOX Red [1]. To assess 3D mitochondrial network morphology we applied SIM (Structured Illumination Microscopy). We compared Jm rates in INS-1E cultivated for 2 hrs at 0 mM, 3 mM, 11 mM and 20 mM glucose. We observed that highest Jm occurs when glucose levels are low and that this is accompanied by noticeable fragmentation of mitochondrial network. Incubation at 0 mM and 3 mM glucose led to 91% and 71% increase in Jm rates, respectively. Incubation of INS-1E cells at 20 mM glucose did not cause any significant change to Jm generation rates and neither was observed any significant change in mitochondrial network structure. Altogether, our data suggest that GSIS has antioxidant character, and is accompanied with mitochondrial network reorganization. Supported by the grant No. 15-02022Y to A.D. from the grant Agency of the Czech Republic. Reference [1] Ježek J, Dlaskova A, Zelenka J, Jabůrek M, Ježek P. H2O2-Activated Mitochondrial Phospholipase iPLA2γ Prevents Lipotoxic Oxidative Stress in Synergy with UCP2, Amplifies Signaling via G-Protein-Coupled Receptor GPR40, and Regulates Insulin Secretion in Pancreatic β-Cells. Antioxid Redox Signal. 2015 23(12):958-72.

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