ADAMTS9, also known as A disintegrin and metalloprotease with thrombospondin type-1 motif, member 9, is a secreted extracellular metalloproteinase. It is involved in various biological processes, such as regulating skeletal muscle insulin sensitivity, primary cilia formation and function, and ovarian development. It may act through pathways like integrin β1 signaling in the context of insulin regulation [1,2,3].

In mouse models, skeletal muscle-specific knockout of Adamts9 led to improved insulin sensitivity. This indicates that ADAMTS9 can regulate insulin sensitivity and signaling in skeletal muscle, potentially through alterations of the integrin β1 signaling pathway and disruption of intracellular cytoskeletal organization [1]. In zebrafish, knockout of adamts9 resulted in abnormal ovarian development, with significantly fewer adult female mutants and abnormal gonadal structures [3].

In conclusion, ADAMTS9 plays essential roles in multiple biological processes. The gene knockout models in mice and zebrafish have revealed its importance in insulin-related metabolic processes and gonadal development. These findings contribute to our understanding of the molecular mechanisms underlying insulin resistance and gonadal development-related disorders [1,3].