技术方法：肥胖症小鼠模型选取2个对其肝脏进行(miRNA)微阵列试验。
结果：miRNA-103 和 miRNA-103 107在肥胖症中高水平表达。沉默这些miRNA，可以改善葡萄糖体内平衡和提高胰岛素敏感性，激活肝脏或脂肪中的miRNA足以扰乱葡萄糖体内平衡。
结论意义：Caveolin-1在胰岛素信号转导途径中是一种参与调控的蛋白，其编码基因是miRNA直接作用的靶基因。这一研究为治疗2-型糖尿病和肥胖症提供一种新的治疗方案。
miRNA-103/107作用的靶基因参与上述信号途径的调控
生物探索推荐英文摘要
doi:10.1038/nature10112
MicroRNAs 103 and 107 regulate insulin sensitivity
Abstract: Defects in insulin signalling are among the most common and earliest defects that predispose an individual to the development of type 2 diabetes1, 2, 3. MicroRNAs have been identified as a new class of regulatory molecules that influence many biological functions, including metabolism4, 5. However, the direct regulation of insulin sensitivity by microRNAs in vivo has not been demonstrated. Here we show that the expression of microRNAs 103 and 107 (miR-103/107) is upregulated in obese mice. Silencing of miR-103/107 leads to improved glucose homeostasis and insulin sensitivity. In contrast, gain of miR-103/107 function in either liver or fat is sufficient to induce impaired glucose homeostasis. We identify caveolin-1, a critical regulator of the insulin receptor, as a direct target gene of miR-103/107. We demonstrate that caveolin-1 is upregulated upon miR-103/107 inactivation in adipocytes and that this is concomitant with stabilization of the insulin receptor, enhanced insulin signalling, decreased adipocyte size and enhanced insulin-stimulated glucose uptake. These findings demonstrate the central importance of miR-103/107 to insulin sensitivity and identify a new target for the treatment of type 2 diabetes and obesity.
