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A new member of the cyclin family cyclin Y (CCNY) is involved in the regulation of various physiological processes. In this study, the role of CCNY in energy metabolism was characterized. We found that compared with wild-type (WT) mice,  Ccny  knockout (KO) mice had both lower body weight and lower fat content. The  Ccny  KO mice also had a higher metabolic rate, resisted the stress of a high-fat diet, and were sensitive to calorie restriction. The expression levels of UCP1 and PGC1α were significantly higher in the brown adipose tissue (BAT) of the  Ccny  KO mice than that of the WT littermate controls, whereas there was no significant difference in BAT weight between the WT and the  Ccny  KO mice. In addition, the down-regulation of  Ccny  resulted in suppression of white adipocyte differentiation both  in vivo  and  in vitro , while the expression of  Ccny  was up-regulated by C/EBPα. Furthermore, both hepatocytes and HepG2 cells that were depleted of  Ccny  were insensitive to insulin stimulation, consistent with the significant inhibition of insulin sensitivity in the liver of the  Ccny  KO mice, but no significant changes in WAT and muscle, indicating that CCNY is involved in regulating the hepatic insulin signaling pathway. The hepatic insulin resistance generated by  Ccny  depletion resulted in down-regulation of the sterol-regulatory element-binding protein (SREBP1) and fatty acid synthase (FASN). Together, these results provide a new link between CCNY and lipid metabolism in mice, and suggest that inhibition of CCNY may offer a therapeutic approach to obesity and diabetes.

Cyclin Y Is Involved in the Regulation of Adipogenesis and Lipid Production