PPARA and non-small cell lung carcinoma: PPAR-α suppression and increased gluconeogenesis in hepatic metabolism have been shown to be the cause of reduced serum ketones in a mouse model of NSCLC, whereas the restoration of ketone production in liver cells via PPAR-α agonist agent (fenofibrate) prevented weight loss and attenuated the degradation of type II muscle fibers compared to control fasted mouse [109].