PMID:12910269

Citation	Zhou, Z, Yon Toh, S, Chen, Z, Guo, K, Ng, CP, Ponniah, S, Lin, SC, Hong, W and Li, P (2003) Cidea-deficient mice have lean phenotype and are resistant to obesity. Nat. Genet. 35:49-56
Abstract	The thermogenic activity of brown adipose tissue (BAT), important for adaptive thermogenesis and energy expenditure, is mediated by the mitochondrial uncoupling protein1 (Ucp1) that uncouples ATP generation and dissipates the energy as heat. We show here that Cidea, a protein of unknown function sharing sequence similarity with the N-terminal region of DNA fragmentation factors Dffb and Dffa, is expressed at high levels in BAT. Cidea-null mice had higher metabolic rate, lipolysis in BAT and core body temperature when subjected to cold treatment. Notably, Cidea-null mice are lean and resistant to diet-induced obesity and diabetes. Furthermore, we provide evidence that the role of Cidea in regulating thermogenesis, lipolysis and obesity may be mediated in part through its direct suppression of Ucp1 activity. Our data thus indicate a role for Cidea in regulating energy balance and adiposity.
Links	PubMed Online version:10.1038/ng1225
Keywords	Adipose Tissue, Brown/physiology; Animals; Apoptosis Regulatory Proteins; Blood Glucose/metabolism; Body Temperature; Carrier Proteins/antagonists & inhibitors; Carrier Proteins/metabolism; Cloning, Molecular; Fatty Acids, Nonesterified/blood; Humans; Ion Channels; Lipolysis; Membrane Proteins/antagonists & inhibitors; Membrane Proteins/metabolism; Mice; Mice, Knockout; Mitochondrial Proteins; Obesity; Phenotype; Proteins/genetics; Proteins/physiology; Thinness/genetics; Triglycerides/blood
edit table

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
edit table

References

See Help:References for how to manage references in GONUTS.