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首页> 美国卫生研究院文献>Biochemical Journal >Substrates of semicarbazide-sensitive amine oxidase co-operate with vanadate to stimulate tyrosine phosphorylation of insulin-receptor-substrate proteins phosphoinositide 3-kinase activity and GLUT4 translocation in adipose cells.
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Substrates of semicarbazide-sensitive amine oxidase co-operate with vanadate to stimulate tyrosine phosphorylation of insulin-receptor-substrate proteins phosphoinositide 3-kinase activity and GLUT4 translocation in adipose cells.

机译：氨基脲敏感的胺氧化酶的底物与钒酸盐协同作用以刺激脂肪细胞中胰岛素受体底物蛋白的酪氨酸磷酸化磷酸肌醇3激酶活性和GLUT4易位。

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It has been shown that the combination of benzylamine or tyramine and low concentrations of vanadate markedly stimulates glucose transport in rat adipocytes by a mechanism that requires semicarbazide-sensitive amine oxidase (SSAO) activity and H(2)O(2) formation. Here we have further analysed the insulin-like effects of the combination of SSAO substrates and vanadate and we have studied the signal-transduction pathway activated in rat adipocytes. We found that several SSAO substrates (benzylamine, tyramine, methylamine, n-decylamine, histamine, tryptamine or beta-phenylethylamine), in combination with low concentrations of vanadate, stimulate glucose transport in isolated rat adipocytes. Furthermore, SSAO substrates together with vanadate stimulated the recruitment of GLUT4 to the cell surface in isolated rat adipocytes. Benzylamine plus vanadate also stimulated glucose transport and GLUT4 translocation in 3T3-L1 adipocytes. Benzylamine or tyramine in combination with vanadate potently stimulated the tyrosine phosphorylation of both insulin receptor substrate (IRS)-1 and IRS-3. In contrast, benzylamine and vanadate caused only a weak stimulation of insulin receptor kinase. Benzylamine or tyramine in combination with vanadate also stimulated phosphoinositide 3-kinase activity; wortmannin abolished the stimulatory effect of benzylamine and vanadate on glucose transport in adipose cells. Furthermore, the administration of benzylamine and vanadate in vivo caused a rapid lowering of plasma glucose levels, which took place in the absence of alterations in plasma insulin. On the basis of these results we propose that SSAO activity regulates glucose transport in adipocytes. SSAO oxidative activity stimulates glucose transport via the translocation of GLUT4 carriers to the cell surface, resulting from a potent tyrosine phosphorylation of IRS-1 and IRS-3 and phosphoinositide 3-kinase activation. Our results also indicate that substrates of SSAO might regulate glucose disposal in vivo.
机译：已经表明，苄胺或酪胺与低浓度的钒酸盐的组合通过需要半氨基甲酸酯敏感的胺氧化酶（SSAO）活性和H（2）O（2）形成的机制显着刺激了大鼠脂肪细胞中的葡萄糖转运。在这里，我们进一步分析了SSAO底物和钒酸盐组合的胰岛素样作用，并研究了在大鼠脂肪细胞中激活的信号转导途径。我们发现几种SSAO底物（苄胺，酪胺，甲胺，正癸胺，组胺，色胺或β-苯乙胺）与低浓度的钒酸盐结合，可刺激离体大鼠脂肪细胞中的葡萄糖转运。此外，SSAO底物与钒酸盐一起刺激了GLUT4在分离的大鼠脂肪细胞中募集到细胞表面。苄胺加钒酸盐还刺激3T3-L1脂肪细胞中的葡萄糖转运和GLUT4易位。苄胺或酪胺与钒酸盐的结合可有效刺激胰岛素受体底物（IRS）-1和IRS-3的酪氨酸磷酸化。相反，苄胺和钒酸盐仅引起胰岛素受体激酶的弱刺激。苄胺或酪胺与钒酸盐的结合也刺激了磷酸肌醇3-激酶的活性。渥曼青霉素取消了苄胺和钒酸盐对脂肪细胞葡萄糖转运的刺激作用。此外，在体内施用苄胺和钒酸盐引起血浆葡萄糖水平的快速降低，这是在血浆胰岛素没有改变的情况下发生的。根据这些结果，我们建议SSAO活性调节脂肪细胞中的葡萄糖转运。由于IRS-1和IRS-3的强酪氨酸磷酸化以及磷酸肌醇3-激酶的活化，SSAO的氧化活性通过GLUT4载体向细胞表面的转运刺激了葡萄糖的转运。我们的结果还表明，SSAO的底物可能会调节体内的葡萄糖处置。

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