Abstract 1212 Copper deficiency by excess fatty acids promote lipotoxicity

Copper (Cu) is an essential cofactor of several enzymes, including cytochrome oxidase (CCO), superoxide dismutase 1 (SOD1), and ceruloplasmin (Cp). These Cu-requiring enzymes play critical roles in metabolism, and patients and animal models with metabolic dysfunction-associated steatotic liver disease (MASLD) present low Cu levels in the liver. Therefore, Cu deficiency in the liver may be the cause or a contributing factor of MASLD displaying high variation in its progression from steatosis to inflammation, fibrosis, cirrhosis, and liver dysfunction.