CIDEC, also known as cell death-inducing DFF45-like effector C or cell death-inducing DNA fragmentation factor-α-like effector C, is a lipid droplet-associated protein. It plays a crucial role in lipid metabolism, regulating processes such as lipid deposition, secretion, and lipolysis [2,4]. It is involved in maintaining systemic glucose homeostasis and is associated with pathways related to insulin sensitivity [2,3]. Genetic models, like transgenic and knockout mouse models, have been instrumental in studying CIDEC's functions.

CIDEC gene silencing in a type 2 diabetic rat model reversed aortic inflammation and remodeling, suggesting it could be a therapeutic target for diabetic vascular complications [1]. In transgenic mouse models, adipose-specific expression of human CIDEC protected against high-fat diet-induced glucose intolerance and regulated lipid metabolism by interacting with adipose triglyceride lipase's activator, CGI-58 [2]. In a small intestine-specific CIDEC knockout (SI-CIDEC-/-) mouse model, knockout mice had lower body weight, less body fat mass, and reduced liver triglycerides, along with alleviated hepatic steatosis and fatty liver inflammation when fed a high-fat diet. This indicates CIDEC in the small intestine accelerates phosphatidic acid synthesis to promote triglyceride accumulation [5].

In conclusion, CIDEC is a key regulator in lipid metabolism and glucose homeostasis. Studies using gene knockout and transgenic mouse models have revealed its significance in diabetes-related vascular and metabolic diseases, as well as in obesity and hepatic steatosis. These findings highlight CIDEC as a potential therapeutic target for these disease areas.