The importance of mitochondrial oxidative stress on beta cells in type II diabetes

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We aim to study natural mechanisms that protect people from diabetes in the beta cells that make insulin. This will help design treatments that may prevent people from developing diabetes. Mitochondria are small parts of cells that generate energy. They also generate damaging by-products called free radicals, that are inactivated by an enzyme called superoxide dismutase (SOD). Mitochondria have their own DNA, mtDNA, a blueprint for proteins needed to make energy. Variations in mtDNA make diabetes more likely by reducing the energy supplied to the beta cells. We will use molecular techniques to lower SOD levels in cultured beta cells and determine whether this increases levels of the damaging free radicals. We will determine whether these changes decrease insulin production, as this would make diabetes likely. Once beta cells are damaged they cannot readily be regenerated and this causes insulin deficiency. Our results may suggest novel treatments with drugs that counteract free radicals to prevent failure of the beta cells. Finding a treatment to prevent this damage would change how we treat patients whose mtDNA predisposes them to diabetes. This includes 140,000 diabetics in the UK and ~95% of people in Polynesia, where diabetes is very common.