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

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，抑制这些细胞中的可的松作用，导致这种药物对燃料代谢(如葡萄糖和血脂水平)的负面副作用显著减少。目前的目标是调查这一途径是如何参与可的松诱导的肥胖和糖尿病的。

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.