...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell metabolism >Cytosolic phosphoenolpyruvate carboxykinase does not solely control the rate of hepatic gluconeogenesis in the intact mouse liver.
【24h】

Cytosolic phosphoenolpyruvate carboxykinase does not solely control the rate of hepatic gluconeogenesis in the intact mouse liver.

机译：胞质磷酸烯醇丙酮酸羧激酶并不仅仅控制完整小鼠肝脏中肝糖异生的速率。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

When dietary carbohydrate is unavailable, glucose required to support metabolism in vital tissues is generated via gluconeogenesis in the liver. Expression of phosphoenolpyruvate carboxykinase (PEPCK), commonly considered the control point for liver gluconeogenesis, is normally regulated by circulating hormones to match systemic glucose demand. However, this regulation fails in diabetes. Because other molecular and metabolic factors can also influence gluconeogenesis, the explicit role of PEPCK protein content in the control of gluconeogenesis was unclear. In this study, metabolic control of liver gluconeogenesis was quantified in groups of mice with varying PEPCK protein content. Surprisingly, livers with a 90% reduction in PEPCK content showed only a approximately 40% reduction in gluconeogenic flux, indicating a lower than expected capacity for PEPCK protein content to control gluconeogenesis. However, PEPCK flux correlated tightly with TCA cycle activity, suggesting that under some conditions in mice, PEPCK expression must coordinate with hepatic energy metabolism to control gluconeogenesis.
机译：当饮食中的碳水化合物不可用时，通过肝脏中的糖异生作用会产生支持重要组织代谢所需的葡萄糖。磷酸烯醇丙酮酸羧激酶（PEPCK）的表达通常被认为是肝脏糖异生的控制点，通常通过循环激素来调节以适应全身性葡萄糖需求。但是，该法规在糖尿病患者中无效。由于其他分子和代谢因素也可以影响糖异生，因此尚不清楚PEPCK蛋白含量在糖异生控制中的明确作用。在这项研究中，量化了具有不同PEPCK蛋白含量的小鼠组中肝脏糖异生的代谢控制。出人意料的是，PEPCK含量降低90％的肝脏显示糖异生通量仅降低约40％，表明PEPCK蛋白含量控制糖异生的能力低于预期。然而，PEPCK通量与TCA循环活性紧密相关，这表明在某些条件下，小鼠中PEPCK的表达必须与肝能量代谢协调以控制糖异生。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号