MOLECULAR CONTROL OF GLUCOSE METABOLISM

葡萄糖代谢的分子控制

• 批准号: 7724102
• 负责人: KOSAKU UYEDA
• 金额: $ 1.05万
• 依托单位: UT SOUTHWESTERN MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-09-01 至 2009-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7724102
• 关键词: Binding Proteins; Biochemical; Carbohydrates; Collaborations; Computer Retrieval of Information on Scientific Projects Database; Diet; Enzyme Gene; Enzymes; Fatty acid glycerol esters; Funding; Genes; Genetic Transcription; Glycolysis; Grant; Institution; Insulin; Intake; Liver; Molecular; Mus; Organ; Oxidation-Reduction; Pancreas; Purpose; Pyruvate; Pyruvates; Research; Research Personnel; Resources; Response Elements; Signal Transduction; Source; Starch; United States National Institutes of Health; feeding; glucose metabolism; lipid biosynthesis; response; transcription factor

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. However, carbohydrates also stimulate transcription of the same genes independent of insulin. The mechanism by which metabolizable carbohydrate generates a signal to induce the transcription of lipogenic enzyme genes became clearer with discovery of the transcription factor termed carbohydrate response element binding protein (ChREBP). The purpose of this collaboration is (a) to determine the biochemical mechanism for the reduced REDOX state of liver of ChREBP-/-, and (b) to determine the source of pyruvate in the liver of ChREBP-/- mice fed high starch diet.

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。然而，碳水化合物也刺激不依赖于胰岛素的相同基因的转录。随着转录因子碳水化合物反应元件结合蛋白(ChREBP)的发现，可代谢碳水化合物产生信号诱导成脂酶基因转录的机制变得更加清晰。这项合作的目的是(A)确定ChREBP-/-肝脏氧化还原状态降低的生化机制，以及(B)确定喂食高淀粉饲料的ChREBP-/-小鼠肝脏中丙酮酸的来源。