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 various physiological processes such as lipid metabolism, adipogenesis, and redox homeostasis, and is associated with pathways like the cAMP/PKA/CREB signaling pathway [3,4]. Genetic models, especially KO/CKO 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) has the opposite effects. Cdo1 tethers Camkk2 to AMPK, activating the AMPK signaling pathway, which promotes fatty acid oxidation and mitochondrial biogenesis to attenuate hepatosteatosis [1]. Adipose-specific knockout of Cdo1 in mice impairs energy expenditure, cold tolerance, and lipolysis, exacerbating diet-induced obesity (DIO) [2].

In conclusion, Cdo1 plays essential roles in regulating lipid metabolism, energy expenditure, and metabolism-related processes. Studies using Cdo1 KO/CKO mouse models have revealed its significance in NAFLD and obesity-related disease areas, providing insights into the underlying molecular mechanisms and potential therapeutic targets.