Mitochondrial mutations can cause a variety of pathologic changes and lead to severe diseases like diabetes, Alzheimer, Parkinson and aging. The aim of this study was to investigate the effects of the mitochondrial mt-Atp8 mutation on ROS production and antioxidative defense. The impact of a life long high fat diet (60 % of the calories from fat) on glucose and lipid metabolisms as well as lipoinflammation were assessed in the conplastic mouse model B6-mtFVB.
The Atp8 subunit supports the assembling of ATP Synthase, which is essential for ATP synthesis in the mitochondrium. The mt-Atp8 mutation caused increased ROS production in liver, muscle and brain. A life long high fat diet caused early severe disturbance in the glucose homeostasis, despite occurrence of adaptional processes. As a result, metabolic and oxidative stress contributed to a reduced life span of the B6-mtFVB mouse strain.