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Synergistic effect of arachidonic acid and cyclic AMP on glucose transport in 3T3-L1 adipocytes.

机译:花生四烯酸和环状AMP对3T3-L1脂肪细胞中葡萄糖转运的协同作用。

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The combined effect of arachidonic acid and cAMP on glucose transport was examined in 3T3-L1 adipocytes. In cells pre-treated with arachidonic acid and increasing concentrations of 8-bromo cAMP for 8 h, although either agent alone enhanced glucose uptake, the simultaneous presence of both agents dramatically increased 2-deoxyglucose uptake in a synergistic fashion. Insulin-stimulated glucose transport, on the other hand, was only slightly affected. The synergistic effect of these two agents was abolished in the presence of cycloheximide. Immunoblot analysis revealed that the contents of ubiquitous glucose transporter (GLUT1) in total cellular and plasma membranes were similarly augmented in cells pre-treated with both arachidonic acid and 8-bromo cAMP, to a greater extent than the additive effect of each agent alone. The content of GLUT4, on the other hand, was not altered under the same experimental conditions. In cells pre-treated with 4beta-phorbol 12beta-myristate 13alpha-acetate (PMA) for 24 h to down-regulate protein kinase C (PKC), the subsequent synergistic effect of arachidonic acid and 8-bromo cAMP was greatly inhibited. In addition, pre-treatment with both PMA and 8-bromo cAMP enhanced glucose transport in a similarly synergistic fashion. Thus the present study seems to indicate that arachidonic acid may act with cAMP in a synergistic way to increase glucose transport by a PKC-dependent mechanism. The increased activity may be accounted for by increased GLUT1 synthesis.
机译:在3T3-L1脂肪细胞中检查了花生四烯酸和cAMP对葡萄糖转运的联合作用。在用花生四烯酸和增加浓度的8-溴cAMP预处理8小时的细胞中,尽管单独使用任何一种试剂都能提高葡萄糖吸收,但同时存在两种试剂会以协同方式显着提高2-脱氧葡萄糖的吸收。另一方面,胰岛素刺激的葡萄糖转运仅受到轻微影响。在环己酰亚胺的存在下,这两种药物的协同作用被消除。免疫印迹分析显示,在用花生四烯酸和8-溴cAMP预处理的细胞中,总细胞膜和质膜中普遍存在的葡萄糖转运蛋白(GLUT1)的含量类似地增加,其程度大于每种单独药物的累加作用。另一方面,在相同的实验条件下,GLUT4的含量没有改变。在用4β-佛波醇12β-肉豆蔻酸酯13α-乙酸酯(PMA)预处理24小时以下调蛋白激酶C(PKC)的细胞中,花生四烯酸和8-溴cAMP的后续协同作用被大大抑制。此外,PMA和8-溴cAMP的预处理均以类似的协同方式增强了葡萄糖的转运。因此,本研究似乎表明花生四烯酸可以与PKAMP协同作用,通过PKC依赖性机制增加葡萄糖的转运。活性增加可能是由于GLUT1合成增加所致。

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