Cdo1, also known as cysteine dioxygenase type 1, is a key enzyme in cysteine catabolism and taurine synthesis, belonging to the mammalian non-heme Fe(II) dioxygenases family [3,4]. It is highly expressed in multiple tissues like liver, adipose tissue, pancreas, etc. Cdo1 is involved in numerous physiological processes such as lipid metabolism, adipogenesis, and redox homeostasis, and plays a role in pathophysiological processes like tumor progression [4]. Genetic models, such as gene knockout mouse models, are valuable for studying its functions.

In mice, hepatocyte-specific knockout of Cdo1 (Cdo1LKO) decreases basal metabolic rate and impairs exercise-induced protection against non-alcoholic fatty liver disease (NAFLD), while hepatocyte-specific overexpression (Cdo1LTG) increases basal metabolic rate and synergizes with exercise to ameliorate NAFLD. Cdo1 tethers Camkk2 to AMPK, activating AMPK signaling, promoting fatty acid oxidation and mitochondrial biogenesis in hepatocytes to attenuate hepatosteatosis [1]. Adipose-specific knockout of Cdo1 in mice impairs energy expenditure, cold tolerance, and lipolysis, exacerbates diet-induced obesity (DIO), and decreases adipose expression of key lipolytic genes, while transgenic overexpression of Cdo1 shows better cold tolerance, ameliorated DIO, and higher lipolysis capacity [2].

In conclusion, Cdo1 plays essential roles in lipid metabolism and energy regulation as revealed through mouse model-based research. In the context of NAFLD and obesity, Cdo1 knockout mouse models have demonstrated its significance in these disease areas, highlighting its potential as a therapeutic target for related metabolic disorders.