Ceramide metabolism and ER stress in fatty-acid mediated destruction of pancreatic beta cells

脂肪酸介导的胰腺β细胞破坏中的神经酰胺代谢和内质网应激

• 批准号: nhmrc : 596828
• 负责人: Prof Trevor Biden
• 金额: $ 36.61万
• 依托单位: Garvan Institute of Medical Research
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2010
• 资助国家: 澳大利亚
• 起止时间: 2010-01-01 至 2012-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/ceramide-metabolism-er-beta-cells/98971
• 关键词: Ceramide; metabolism; ER; stress; fatty

The underlying cause of Type 2 diabetes is the failure of pancreatic beta cells to secrete sufficient insulin to overcome the insulin resistance that is associated with obesity. Beta cell failre is associated with both defective insulin secretion and loss of beta cell mass. This proposal focuses on the cellular mechanisms and stress pathways whereby too much fatty acid promotes beta cell death.

2型糖尿病的根本原因是胰腺β细胞不能分泌足够的胰岛素来克服与肥胖相关的胰岛素抵抗。β细胞衰竭与胰岛素分泌缺陷和β细胞质量损失有关。这项提案的重点是细胞机制和应激途径，过多的脂肪酸促进β细胞死亡。