LIPID METABOLISM BY NMR

通过 NMR 检测脂质代谢

• 批准号: 8361204
• 负责人: FARIBA M ASSADI-PORTER
• 金额: $ 0.07万
• 依托单位: UNIVERSITY OF WISCONSIN-MADISON
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-03-01 至 2012-02-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8361204
• 关键词: Coenzyme A; Development; Diet; Disease; Fatty Liver; Funding; Genes; Goals; Grant; Hepatic; Human; Insulin Resistance; Lipids; Mediating; Metabolic; Metabolic Diseases; Metabolic syndrome; Metabolism; Monounsaturated Fatty Acids; Mus; National Center for Research Resources; Obesity; Pathway interactions; Principal Investigator; Protein Isoforms; Research; Research Infrastructure; Resistance; Resources; Rodent; Role; Source; Stearoyl-CoA Desaturase; Stress; United States National Institutes of Health; biological adaptation to stress; cost; insight; lipid biosynthesis

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The long-term goal of this application is to understand the role of stearoyl-CoA desaturase in metabolism. Stearoyl-CoA desaturase (SCD) is a critical regulator of lipogenesis that catalyzes the synthesis of monounsaturated fatty acids (MUFA), mainly oleoyl- (18:1n9) and palmitoleoyl-CoA (16:1n7). SCD expression is elevated in human and rodent obese and insulin resistant states, suggesting that excess 18:1n9 or 16:1n7 synthesis may contribute to metabolic disease development. Mice with a global deletion of the SCD1 isoform are remarkably resistant to diet- and genetically-induced obesity, insulin resistance and liver steatosis. In this project we will focus on two aims. In Aim 1, we will determine the contribution of hepatic SCD1 expression to the ER stress response and ER stress-mediated lipogenesis. In Aim 2, we will determine the mechanisms causing ER stress due to SCD1 deficiency. As the main metabolic culprits in diseases of the metabolic syndrome are lipids, understanding the role of stearoyl-CoA desaturase genes in hepatic metabolism and ER stress pathways might provide major insights

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， NCRR赠款不直接向子项目或子项目工作人员提供资金。 本申请的长期目标是了解硬脂酰辅酶A去饱和酶在代谢中的作用。硬脂酰辅酶A去饱和酶（SCD）是脂肪生成的关键调节因子，催化单不饱和脂肪酸（MUFA）的合成，主要是油酰-（18：1 n9）和棕榈油酰辅酶A（16：1 n7）。SCD表达在人类和啮齿动物肥胖和胰岛素抵抗状态中升高，表明过量的18：1 n9或16：1 n7合成可能有助于代谢疾病的发展。具有SCD 1同种型整体缺失的小鼠对饮食和遗传诱导的肥胖、胰岛素抵抗和肝脏脂肪变性具有显著抗性。在这个项目中，我们将专注于两个目标。在目标1中，我们将确定肝SCD 1表达对ER应激反应和ER应激介导的脂肪生成的贡献。在目标2中，我们将确定由于SCD 1缺陷引起ER应激的机制。由于代谢综合征疾病的主要代谢罪魁祸首是脂质，因此了解硬脂酰CoA去饱和酶基因在肝脏代谢和ER应激途径中的作用可能会提供重要的见解