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

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的主要研究者可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 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。 该应用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，可催化单不饱和脂肪酸 (MUFA) 的合成，主要是油酰辅酶 A (18:1n9) 和棕榈酰辅酶 A (16:1n7)。 SCD 表达在人类和啮齿类动物肥胖和胰岛素抵抗状态下升高，表明过量的 18:1n9 或 16:1n7 合成可能会导致代谢性疾病的发生。 SCD1亚型整体缺失的小鼠对饮食和遗传引起的肥胖、胰岛素抵抗和肝脏脂肪变性具有显着的抵抗力。在这个项目中，我们将重点关注两个目标。在目标 1 中，我们将确定肝脏 SCD1 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 SCD1 缺陷导致 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，了解硬脂酰辅酶A去饱和酶基因在肝脏代谢和内质网应激途径中的作用可能会提供重要的见解