Deficiency of carbohydrate response element-binding protein (ChREBP) reduces lipogenesis as well as glycolysis
Deficiency of carbohydrate response element-binding protein (ChREBP) reduces lipogenesis as well as glycolysis
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DOI：
10.1073/pnas.0401516101
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发表时间：
2004-05-11
影响因子：
11.1
通讯作者：
Uyeda, K
中科院分区：
文献类型：
--
作者：
Iizuka, K;Bruick, RK;Uyeda, K
肝脏通过将多余的碳水化合物转化为脂肪储存来满足身体的长期能量需求。胰岛素是促进肝脏脂肪生成的因素之一，但越来越多的证据表明，葡萄糖也有助于通过独立于胰岛素的机制协调调节肝脏中的碳水化合物和脂肪代谢。在这项研究中，我们表明，转录因子，碳水化合物反应元件结合蛋白（ChREBP），是必需的基础和碳水化合物诱导的几种肝酶的表达协调控制葡萄糖代谢，脂肪酸，脂肪酸和甘油三酯在体内的合成。
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.