基于前期研究，即发现幽门螺杆菌(Hp)感染可引起胰岛素抵抗，糖尿病患者Hp感染率明显增加（Diabetes Res Clin Pract, 2013）。随后发现Hp阳性小鼠血糖水平增高，合并Hp感染的糖尿病小鼠胰岛素抵抗标志物HOMA-IR明显异常。进一步机制研究表明，Hp感染可降低IRS-1等胰岛素信号通路分子的磷酸化，增加转录因子c-Jun和细胞因子信号转导抑制因子3（SOCS3）的表达。结合我们的芯片结果，即Hp感染可使lncRNA-AK096550表达降低，由此我们提出Hp通过调控c-Jun/lnc-AK096550诱导SOCS3从而引起胰岛素抵抗的科学假说。本研究拟利用胰岛素钳夹实验、RNA干扰、RIP、RNA pull down、报告基因分析等手段来阐明c-Jun/lnc-AK096550/SOCS3在Hp致胰岛素抵抗中的作用，为Hp与糖尿病关系的研究提供新的理论依据。

Based on our previous findings，we found that Helicoabcter pylori (Hp) infection increased the risk of insulin resistance and patients with insulin resistance or diabetes had a higher rate of Hp infection. We also found that chronic Hp-infected mice had a higher blood glucose level than controls and the metabolic indexes such as HOMA-IR were more abnormal in diabetic mice with Hp infection than in diabetic mice without Hp infection. We further investigate the downstream molecular mechanisms of Hp induced insulin resistance.In vitro studies showed that Hp infection could down-regulate the phosphorylation of insulin signaling proteins and increase SOCS3 and transcription factor c-Jun expression.Our microarray analysis found that Hp infection could alter various kinds of lncRNA expression. Thus we put forward a scientific hypothesis that Hp infection can lead to insulin resistance via c-Jun/AK096550/SOCS3 pathway. By use of RNA interference, RNA pull down assay, Reporter assay, RNA immunoprecipitation,etc., this project will confirm that the relationship between Hp infection and insulin resistance and the role of c-Jun/AK096550/SOCS3 pathway in Hp-induced insulin resistance. It will provide a new theoretical basis for the molecular mechanism of Hp infection and extragastrointestinal diseases.