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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 当碳水化合物的摄入量超过对能量的短期要求时，将其存储为脂肪。 肝脏是负责过量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可诱导与糖酵解和脂肪合成有关的十多种酶的基因转录。 由胰腺分泌的胰岛素对碳水化合物分泌，通过激活脂肪生成酶表达来促进脂肪生成。 但是，碳水化合物还刺激与胰岛素无关的相同基因的转录。 随着发现称为碳水化合物响应元件的结合蛋白（CHREBP）的转录因子，可代谢碳水化合物生成诱导脂肪酶基因转录的信号变得更加清晰。 该协作的目的是（a）确定Chrebp-/ - 和（b）降低的氧化还原状态的生化机制，以确定Chrebp - / - 小鼠喂养高淀粉饮食的丙酮酸的来源。