Regulation of skeletal muscle mitochondrial biogenesis by GSK-3β

Our muscles have the remarkable ability to adapt to changing circumstances. This means that both muscle mass and muscle metabolism can normally adapt well to changes in, among other things, the degree of physical activity or muscle strain. The involvement of GSK-3β in the molecular regulation of muscle mass has previously already been demonstrated. For this dissertation, the role of GSK-3β in the regulation of muscle metabolism and in particular the production of mitochondria (mitochondrial biogenesis) was investigated. The outcome of this research is that inhibiting GSK-3β leads to an increased expression of PGC-1α which activates TFEB and subsequently causes mitochondrial biogenesis. This dissertation describes new insights in the regulation of muscle metabolism that can be important in the treatment of patients whose muscle metabolism is affected.