The influence of cortisone on the synthesis and signaling of osteoblastic-derived mediators of metabolic dysfunction.

可的松对成骨细胞衍生的代谢功能障碍介质的合成和信号传导的影响。

• 批准号: nhmrc : 1013295
• 负责人: Dr Tara Speranza
• 金额: $ 21.71万
• 依托单位: Australian National University
• 依托单位国家: 澳大利亚
• 项目类别: Early Career Fellowships
• 财政年份: 2011
• 资助国家: 澳大利亚
• 起止时间: 2011-01-01 至 2017-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/influence-cortisone-synthesis-metabolic-dysfunction/109707
• 关键词: influence; cortisone; synthesis; signaling; osteoblastic

Long-term use of cortisone (glucocorticoids) often leads to significant health problems such as diabetes and obesity. We have convincing preliminary data suggesting these side effects are, at least in part, mediated via bone cells. Inhibiting cortisone action in these cells, in mice treated with cortisone, results in a significant reduction of the negative side effects of this drug on fuel metabolism (eg glucose and lipid levels). The current aim is to investigate how this pathway is involved in cortisone-induced obesity and diabetes.

长期使用可的松（糖皮质激素）往往会导致严重的健康问题，如糖尿病和肥胖症。我们有令人信服的初步数据表明，这些副作用至少部分是通过骨细胞介导的。在用可的松治疗的小鼠中，抑制可的松在这些细胞中的作用，导致该药物对燃料代谢（例如葡萄糖和脂质水平）的负面副作用显著减少。目前的目标是研究这一途径是如何参与可的松诱导的肥胖和糖尿病。