Wei Yuren, Wang Dong, Topczewski Farran, Pagliassotti Michael J
Department of Food Science and Human Nutrition, Colorado State University, Fort Collins, CO 80523, USA.
J Nutr Biochem. 2007 Jan;18(1):1-9. doi: 10.1016/j.jnutbio.2006.03.013. Epub 2006 Jul 18.
Organisms reprogram metabolic pathways to adapt to changes in nutrient availability. This requires that nutrient-based stimuli are sensed, signals are transmitted, and highly specific responses are engaged. We propose that in the liver, the mitogen-activated protein kinase, c-jun N-terminal kinase (JNK), links excessive nutrient metabolism with impaired insulin regulation of glucose production. The liver, by virtue of its anatomic position and selective regulatory features, buffers and is highly responsive to changes in nutrient delivery. In particular, sugars such as sucrose and fructose uniquely regulate and are selectively metabolized by the liver. We propose that when hepatic fructose uptake exceeds requirements for glycogen and energy (hepatic sugar excess), the JNK-signaling pathway is engaged as part of the adaptive response.
生物体通过重新编程代谢途径来适应营养物质可利用性的变化。这需要感知基于营养物质的刺激、传递信号并引发高度特异性的反应。我们提出，在肝脏中，丝裂原活化蛋白激酶c-Jun氨基末端激酶（JNK）将过量的营养物质代谢与胰岛素对葡萄糖生成的调节受损联系起来。肝脏凭借其解剖位置和选择性调节特性，缓冲并对营养物质输送的变化高度敏感。特别是，蔗糖和果糖等糖类对肝脏具有独特的调节作用，并被肝脏选择性代谢。我们提出，当肝脏果糖摄取量超过糖原和能量需求（肝脏糖分过剩）时，JNK信号通路作为适应性反应的一部分被激活。
