The pathophysiological role of Succinate dehydrogenase deficiency in β-cell aging and diabetes
Aging is a major risk factor for Type 2 Diabetes (T2D), a disease of glucose homeostasis characterized by progressive β-cell failure. Mitochondrial dysfunction is a central contributor to β-cell failure of diabetes, but the underlying mechanism in aging is unclear. Dr. Lee’s research focuses on understanding how the age-dependent evolution of β-cell metabolic behavior leads to diabetes development. The proposed study evaluates the role of a key mitochondrial enzyme, succinate dehydrogenase in age-associated mitochondrial dysfunction, β-cell failure and T2D progression. Identifying a molecular mechanism by which β-cells age and predispose the elderly to T2D has the potential to unveil new therapeutic strategies that target the aging aspect of the disease and are individualized for the older population.
