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该文旨在探讨水通道蛋白7(AQP7)在3T3-L1脂肪细胞不同分化阶段的表达以及其对胰岛素信号通路中蛋白激酶B(PKB)的影响。通过培养3T3-L1前体脂肪细胞,诱导分化为成熟的脂肪细胞,用荧光定量PCR、Western blot、酶学方法分析显示,随3T3-L1脂肪细胞分化过程,AQP7与PKB磷酸化水平同步上升,同时培养基中释放的甘油浓度伴随AQP7的表达平行增加。以TNF-α处理分化成熟的脂肪细胞构建胰岛素抵抗模型,AQP7与PKB磷酸化水平均下降,转染高表达AQP7基因的重组腺病毒载体(Ad-AQP7)之后,随着AQP7表达上调,胰岛素刺激下的PKB磷酸化水平提高,并且葡萄糖代谢能力增强。由此可见,AQP7水平随3T3-L1脂肪细胞分化过程逐渐上升,其高表达可能通过增加PKB磷酸化水平改善胰岛素敏感性,提示AQP7可能成为治疗肥胖的一个重要作用靶点。
This article aims to investigate the expression of aquaporin 7 (AQP7) in different differentiation stages of 3T3-L1 adipocytes and its effect on protein kinase B (PKB) in the insulin signaling pathway. Fluorescence quantitative PCR, Western blot and enzymatic analysis showed that the phosphorylation level of AQP7 and PKB increased synchronously with the differentiation of 3T3-L1 adipocytes during the culture of 3T3-L1 preadipocytes, Simultaneously, the glycerol released in the medium increased in parallel with the expression of AQP7. AQP7 and PKB phosphorylation levels were down-regulated by TNF-α-treated mature adipocytes. After transfected with the recombinant adenovirus vector (Ad-AQP7) that overexpressed AQP7 gene, with the increase of AQP7 expression, insulin stimulation PKB under the phosphorylation level increased, and glucose metabolism increased. Thus, the level of AQP7 increased gradually with the differentiation of 3T3-L1 adipocytes, and its high expression may improve insulin sensitivity by increasing PKB phosphorylation, suggesting that AQP7 may be an important target for the treatment of obesity.