Objective To investigate the role of aquaglyceroporin 7 (AQP7) played in insulin resistance of adipocytes.Methods 3T3-L1 preadipocyte cells were induced to be fully differentiated adipocytes and then insulin resistance was induced by dexamethasone (DXM).Adenovirus vector over-expressing AQP7 (Ad-AQP7) was constructed and transfected into adipocytes.Expression levels of AQP7,glycerol release from adipocytes,changes in glucose consumption,and phosphorylated protein kinase B (p-PKB) were measured.Results 48 h-treatment of dexamethasone significantly inhibited the expression level of p-PKB (P＜0.01) and decreased glucose utilization,as well as down-regulation of AQP7 (P＜0.01).Over-expression of AQP7 by transfecting Ad-AQP7 to dexamethasone (DXM)-induced insulin resistant adipocytes could improve glycerol secretion of adipocytes,being consistent with the restoration of p-PKB expression levels and glucose consumption.Conclusions AQP7 may improve in molecular mechanism of insulin resistance in adipocytes.Overexpression of AQP7 may contribute to the improvement of insulin resistance in adipocytes and might be correlated with better phosphorylation of PKB.%目的 探讨脂肪细胞中水通道蛋白7(AQP7)表达与胰岛素抵抗的关系.方法 培养3T3-L1前体脂肪细胞,诱导分化为成熟的脂肪细胞,并用地塞米松(DXM)处理建立胰岛素抵抗模型.构建Ad-AQP7重组腺病毒,转染胰岛素抵抗的脂肪细胞,检测AQP7表达水平的改变与脂肪细胞甘油释放水平、葡萄糖代谢能力以及磷酸化PKB表达改变的关系,从而阐明AQP7改善胰岛素抵抗的可能机制.结果 100 nmol/L DXM作用分化成熟的脂肪细胞诱导胰岛素抵抗,48 h后p-PKB水平和葡萄糖消耗量明显减少(P＜0.01),为胰岛素抵抗的最佳状态.胰岛素抵抗状态下AQP7 mRNA和蛋白水平明显减少(均P＜0.01).Ad-AQP7腺病毒转染胰岛素抵抗的脂肪细胞72h,随着AQP7表达增加,培养基中甘油释放浓度增加,胰岛素刺激下的p-PKB水平呈现同样上升趋势,并且葡萄糖代谢能力得到明显改善.结论 AQP7可能参与胰岛素抵抗的分子机制;高表达AQP7可改善胰岛素抵抗,其机制可能与PKB信号通路改善有关.
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