Mechanisms of fatty-acid mediated destruction of pancreatic beta cells

脂肪酸介导的胰腺β细胞破坏机制

• 批准号: nhmrc : 376020
• 负责人: A/Pr David Laybutt
• 金额: $ 34.04万
• 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: 2006
• 资助国家: 澳大利亚
• 起止时间: 2006-01-01 至 2008-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/mechanisms-fatty-acid-beta-cells/78271
• 关键词: Mechanisms; fatty; acid; mediated; destruction

Type 2 diabetes is associated with obesity, but not all obese individuals develop the disease. Non-diabetic obese subjects are able to compensate for diminished sensitivity to insulin (a general feature of obesity) by enhanced output of insulin from the pancreatic beta-cells of the islet of Langerhans. In diabetics this compensatory mechanism is disrupted. Obesity and Type 2 diabetes are also associated with elevated levels of fatty acids (FAs) in the bloodstream. These can be taken up by the beta-cells where they exert both short and long-term effects. In the longer term FAs can be toxic to beta-cells and this is thought to be important in the failure of beta-cell compensation. The project is aimed at a better understanding of the manner by which different types of FAs influence the susceptibility of beta-cells to destruction. It builds on our preliminary results suggesting that the capacity of the beta-cell to convert saturated FAs to unsaturated FAs helps protect them from destruction. Our aim is to examine the mechanisms underlying this protection.

2型糖尿病与肥胖有关，但并非所有肥胖者都会患上这种疾病。非糖尿病肥胖受试者能够通过增强胰岛的胰腺β细胞的胰岛素输出来补偿对胰岛素的敏感性降低（肥胖的一般特征）。在糖尿病患者中，这种代偿机制被破坏。肥胖和2型糖尿病也与血液中脂肪酸（FA）水平升高有关。这些可以被β细胞吸收，在那里它们发挥短期和长期的作用。从长远来看，FA可能对β细胞有毒，这被认为是β细胞代偿失败的重要原因。该项目旨在更好地了解不同类型的脂肪酸影响β细胞对破坏的敏感性的方式。它建立在我们的初步结果表明，β-细胞的能力，将饱和脂肪酸不饱和脂肪酸有助于保护他们免受破坏。我们的目的是研究这种保护的机制。