CIDE proteins and metabolic disorders

Purpose of review The cell death-inducing DFF45-like effector (CIDE) family proteins, comprising three members, Cidea, Cideb, and Fsp27 (Cidec), have emerged as important regulators for various aspects of metabolism. This review summarizes our current understanding about the physiological roles of CIDE proteins, their transcriptional regulations, and their underlying mechanism in controlling the development of metabolic disorders. Recent findings Animals with deficiency in Cidea, Cideb, and Fsp27 all display lean phenotypes with higher energy expenditure and are resistant to diet-induced obesity and insulin resistance. CIDE proteins, localized to lipid droplets and endoplasmic reticulum, control lipid metabolism in adipocytes and hepatocytes through regulating AMP-activated protein kinase stability and influencing lipogenesis or lipid droplet formation. The expression of CIDE proteins is controlled at both transcriptional and posttranslational levels and positively correlates with the development of obesity, liver steatosis, and insulin sensitivity in both rodents and humans. Summary CIDE proteins are important regulators of energy homeostasis and are closely linked to the development of metabolic disorders including obesity, diabetes, and liver steatosis. They may serve as potential molecular targets for the screening of therapeutic drugs for these diseases.