HEPATIC MITOCHONDRIAL METABOLISM DURING INSULIN RESISTANCE

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 当碳水化合物摄入量超过短期能量需求时，就会以脂肪的形式储存起来。肝脏是负责将多余的碳水化合物转化为脂肪的主要器官。摄入高碳水化合物饮食会诱导肝脏中十几种酶的基因转录，这些酶参与糖酵解和脂肪合成。胰岛素是胰腺对碳水化合物的反应而分泌的，通过激活造脂酶的表达来促进脂肪生成。本项目的目的是使用2H和13C核磁共振方法来分析各种动物模型和人体受试者肝脏葡萄糖的产生。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. When carbohydrate intake exceeds short-term requirements for energy, it is stored as fat. The liver is the principle organ responsible for the conversion of excess carbohydrate to fat. Ingesting a high carbohydrate diet induces gene transcription of over a dozen enzymes in liver that are involved in glycolysis and fat synthesis. Insulin, secreted by the pancreas in response to carbohydrate promotes lipogenesis by activating lipogenic enzyme expression. The purpose of this project is to use 2H and 13C NMR methods to analyze hepatic production of glucose in a variety of animal models and human subjects.