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Deficiency of carbohydrate response element-binding protein (ChREBP) reduces lipogenesis as well as glycolysis.


ABSTRACT: The liver provides for long-term energy needs of the body by converting excess carbohydrate into fat for storage. Insulin is one factor that promotes hepatic lipogenesis, but there is increasing evidence that glucose also contributes to the coordinated regulation of carbohydrate and fat metabolism in liver by mechanisms that are independent of insulin. In this study, we show that the transcription factor, carbohydrate response element-binding protein (ChREBP), is required both for basal and carbohydrate-induced expression of several liver enzymes essential for coordinated control of glucose metabolism, fatty acid, and the synthesis of fatty acids and triglycerides in vivo.

SUBMITTER: Iizuka K 

PROVIDER: S-EPMC409910 | biostudies-literature | 2004 May

REPOSITORIES: biostudies-literature

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Deficiency of carbohydrate response element-binding protein (ChREBP) reduces lipogenesis as well as glycolysis.

Iizuka Katsumi K   Bruick Richard K RK   Liang Guosheng G   Horton Jay D JD   Uyeda Kosaku K  

Proceedings of the National Academy of Sciences of the United States of America 20040426 19


The liver provides for long-term energy needs of the body by converting excess carbohydrate into fat for storage. Insulin is one factor that promotes hepatic lipogenesis, but there is increasing evidence that glucose also contributes to the coordinated regulation of carbohydrate and fat metabolism in liver by mechanisms that are independent of insulin. In this study, we show that the transcription factor, carbohydrate response element-binding protein (ChREBP), is required both for basal and carb  ...[more]

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