Mitochondrial morphology and function in metabolic excess. Increased metabolic input in the form of high glucose and/or fat (HG/HF) provides an increased entry of reducing equivalents into the ETC resulting in enhanced ΔΨm, favorable for electron slippage and ROS production. Metabolic signaling may alter mitochondrial morphology in HG/HF conditions. Altered mitochondrial morphology under metabolic excess plays a role in ROS production and subsequent mitochondrial dysfunction. Conversely, ROS inside mitochondria causes mitochondrial dysfunction, which may affect mitochondrial morphology. Accumulating damage inside of mitochondria through ROS progressively causes irreversible mitochondrial dysfunction for a new exacerbating cycle of ROS and mitochondrial dysfunction. Apoptosis and dysregulation of mitophagy are accompanied in the metabolic insult conditions, which also interface with mitochondrial morphology change.
