SH2-B调节JAK2在肥胖症发病过程中的分子机制研究
基本信息
结项摘要
利用建立的高效稳定表达瘦素受体细胞株HEK293LRb和SH2-B基因敲除小鼠，通过比较普通和/或高脂饲料喂养SH2-B基因敲除小鼠、杂合子及野生型小鼠能量吸收和能量消耗、体重、血清瘦素等生理学指标和小鼠下丘脑瘦素信号通路中关键分子的活性及效应分子表达的变化，确定SH2-B作为JAK2内源性的增强因子通过JAK2/Stat3和/或JAK2/IRS2/PI3K两通路参与瘦素对能量平衡和体重的调节；进一步改变SH2-B与SOCS3和PTP1B在瘦素受体细胞株HEK239LRb中的表达量和检测衰老及高脂性肥胖小鼠下丘脑上述基因表达率的表化与瘦素敏感性及脂肪生成的关系，确定SH2-B能否拮抗SOCS3和PTP1B对瘦素上述两信号通路和瘦素生物学效应的抑制。这一研究不仅有助于揭示肥胖症发生的机制，而且能为研发控制肥胖症及其相关疾病新药提供靶分子。
项目摘要
项目成果
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数据更新时间：2023-05-31
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