Programme

Preliminary description:
Mitochondria are dynamic organelles that are central for the maintenance of cellular energy homeostasis producing ATP via oxidative phosphorylation (OXPHOS). Obesity and type-2 diabetes are intricately linked to impaired mitochondrial functions. In these diseases the peripheral tissues exhibit fragmented mitochondria with impaired OXPHOS capacity, reduced number and mass, enhanced reactive oxygen species (ROS) and the impaired mitochondrial dynamics. Mitochondrial dysfunction is thought to be a consequence of chronic nutrient excess -induced inflammation and oxidative stress. Based on these pathos-mechanisms, targeting mitochondrial function in metabolically active peripheral tissues are considered as a promising treatment approach for these diseases. Lifestyle modifications remain the first line of treatments for metabolic diseases and mitochondrial defects. Among these, exercise, hypoxia and cold exposure are one of the few proven methods for improving mitochondrial functions. In addition, NAD+ restoration therapy is a key treatment approach that involves boosting NAD+ levels. Our symposium will cover the role of mitochondrial signaling in obesity and type-2 diabetes in peripheral tissues. In addition, boosting mitochondrial health by lifestyle changes, and pharmacotherapy to prevent obesity and type-2 diabetes.