Usurping the mitochondrial supremacy: Extramitochondrial sources of reactive oxygen intermediates and their role in beta cell metabolism and insulin secretion
| Autor: | Emma Heart, Joshua P. Gray |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
Health
Toxicology and Mutagenesis Glucose uptake Mitochondrion Carbohydrate metabolism Biology Toxicology medicine.disease_cause Islets of Langerhans Mice Insulin Secretion mental disorders Benzoquinones medicine Animals Humans Insulin Metabolism Mitochondrial shuttle Mitochondria Rats nervous system diseases Cytosol nervous system Biochemistry Beta cell Reactive Oxygen Species psychological phenomena and processes Oxidative stress |
| Zdroj: | Toxicology Mechanisms and Methods. 20:167-174 |
| ISSN: | 1537-6524 1537-6516 |
| DOI: | 10.3109/15376511003695181 |
| Popis: | Insulin secretion from pancreatic beta cells is a process dependent on metabolism. While oxidative stress is a well-known inducer of beta cell toxicity and impairs insulin secretion, recent studies suggest that low levels of metabolically-derived reactive oxygen intermediates (ROI) also play a positive role in insulin secretion. Glucose metabolism is directly correlated with ROI production, particularly in beta cells in which glucose uptake is proportional to the extracellular concentration of glucose. Low levels of exogenously added ROI or quinones, which stimulate ROI production, positively affect insulin secretion, while antioxidants block insulin secretion, suggesting that ROI activate unidentified redox-sensitive signal transduction components within these cells. The mitochondria are one source of ROI: increased metabolic flux increases mitochondrial membrane potential resulting in electron leakage and adventitious ROI production. A second source of ROI are cytosolic and plasma membrane oxidoreductases which oxidize NAD(P)H and directly produce ROI through the reduction of molecular oxygen. The mechanism of ROI-mediated potentiation of insulin secretion remains an important topic for future study. |
| Databáze: | OpenAIRE |
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