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Mice With a Deletion in the Gene for CCAAT/Enhancer-Binding Protein ß Are Protected Against Diet-Induced Obesity

¹ Department of Nutrition, Case Western Reserve University, Cleveland, Ohio
² Department of Genetics, Case Western Reserve University, Cleveland, Ohio

Address correspondence and reprint requests to Colleen M. Croniger, Department of Nutrition, Case Western Reserve University, Cleveland, OH 44106. E-mail: cmc6{at}case.edu

Abbreviations: ACC, acetyl CoA carboxylase; AOX, acyl-CoA oxidase; BAT, brown adipose tissue; C/EBPß, CCAAT/enhancer-binding protein ß; CPT, carnitine palmitoyltransferase; CRE, cAMP responsive element–binding protein regulatory region; FAS, fatty acid synthase; FFA, free fatty acid; HMG, hydroxymethylglutaryl; LCAD, long acyl-CoA dehydrogenase; PPAR, peroxisome proliferator–activated receptor ; SCD-1, sterol CoA desaturase-1; SREBP-1, sterol regulatory element–binding protein-1; UCP, uncoupling protein

The CCAAT/enhancer-binding protein ß (C/EBPß) is required for adipocyte differentiation and maturation. We have studied the role of the transcription factor, C/EBPß, in the development of diet-induced obesity. Mice with a deletion in the gene for C/EBPß (C/EBPß^–/–) and wild-type mice were fed a high-fat diet (60% fat) for 12 weeks. The C/EBPß^–/– mice lost body fat, whereas the wild-type mice increased their total body fat on a high-fat diet. The C/EBPß^–/– mice had lower levels of blood triglycerides, free fatty acids, cholesterol, and hepatic triglyceride accumulation compared with the wild-type mice, thus protecting them from diet-induced obesity and fatty liver on a high-fat diet. Deletion of C/EBPß gene resulted in greatly reducing hepatic lipogenic genes, acetyl CoA carboxylase, and fatty acid synthase and increasing the expression of ß-oxidation genes in the brown adipose tissue. CO₂ production was significantly higher in the C/EBPß^–/– mice as was the level of uncoupling protein (UCP)-1 and UCP-3 in the muscle. In conclusion, the transcription factor C/EBPß is an important regulator in controlling lipid metabolism and in the development of diet-induced obesity.

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