Microarray expression analysis of Aquaporin-9 (AQP9) knockout effect in fasted C57Bl/6 mice
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Aquaporin-9 is a glycerol, urea and hydrogen peroxide channel, with highest expression in the liver. We have previously demonstrated that AQP9 is required for hepatocyte glycerol uptake and thus for gluconeogenesis from glycerol. AQP9 gene deletion in db/db mice of the C57BLKS background results in improved glycemia, while glycemia in normal mice is unaffected even during starvation, when glycerol is an important gluconeogenic substrate. To identify mechanisms that compensate the lack of glycerol uptake for gluconeogenesis, we performed a gene expression profiling and metabolomics study.
水通道蛋白9(Aquaporin-9)是一种介导甘油、尿素与过氧化氢转运的通道蛋白,在肝脏中表达水平最高。我们既往的研究已证实,AQP9是肝细胞摄取甘油、并通过甘油完成糖异生过程所必需的蛋白。在C57BLKS遗传背景的db/db小鼠中敲除AQP9基因,可改善其血糖水平;而正常小鼠即便在饥饿状态下——此时甘油作为关键的糖异生底物——血糖水平也未受影响。为了阐明代偿甘油摄取缺失以维持糖异生的分子机制,我们开展了基因表达谱分析与代谢组学研究。



