Insulin and insulin-like growth factor-1 modulation of glucose transport in arterial smooth muscle cells: implication of GLUT-4 in the vasculature.
Insulin and insulin-like growth factor-1 modulation of glucose transport in arterial smooth muscle cells: implication of GLUT-4 in the vasculature.
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胰岛素和胰岛素样生长因子-1 对动脉平滑肌细胞中葡萄糖转运的调节：GLUT-4 在脉管系统中的意义。
DOI：
10.1093/ajh/7.4.357
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发表时间：
1994
影响因子：
3.2
通讯作者：
K. Rose
中科院分区：
文献类型：
--
作者：
P. Standley;K. Rose
胰岛素调节血管平滑肌细胞（VSMC）的许多生理过程，如收缩性、增殖和离子稳态。然而，葡萄糖转运的激素调节尚未在这些细胞的纯群体中进行探索。本研究表明，胰岛素和胰岛素样生长因子-1（IGF-1）增加了a7 r5克隆和新鲜制备的Sprague-Dawley主动脉（SDa）VSMC的葡萄糖转运。在a7 r5细胞中，生理（10（-12）至10（-9）mol/L）胰岛素浓度使转运增加8%至15%，而超生理浓度（10（-9）至10（-6）mol/L）使转运增加高达60%（P <0.05，所有测试浓度均无增加）。在SDa细胞中，胰岛素更有效，在10（-8）mol/L时显示70%的最大转运刺激（P <0.05 va 7 r5细胞）。胰岛素对葡萄糖转运的调节是通过蛋白质合成非依赖性途径进行的，10 μ mol/L放线菌酮没有影响。胰岛素在治疗后20分钟内产生这些效应，细胞松弛素B（10 μ mol/L）分别抑制基础和胰岛素刺激的葡萄糖转运93%和96%。用2.5 pg/mL胰岛素受体特异性抗体单独刺激胰岛素受体，可刺激葡萄糖转运20%，表明转运可通过IGF-1受体非依赖性机制刺激。然而，在所研究的两种细胞系中，IGF-1都是更有效的转运刺激剂，在a7 r5和SDa细胞中，最大刺激（10（-8）mol/L IGF-1）分别为60%和80%（在两种细胞系中，P <0.05 v10（-8）mol/L胰岛素）。胰岛素对葡萄糖转运的刺激是[D+]-葡萄糖特异性的; [L-]-葡萄糖不竞争转运。（250字处删节）
Insulin modulates many physiological processes in vascular smooth muscle cells (VSMC) such as contractility, proliferation, and ion homeostasis. However, hormonal modulation of glucose transport has not been explored in pure populations of these cells. This study demonstrates that insulin and insulin-like growth factor-1 (IGF-1) increase glucose transport in a7r5 clonal and freshly prepared Sprague-Dawley aortic (SDa) VSMC. In a7r5 cells, physiologic (10(-12) to 10(-9) mol/L) insulin concentrations increase transport by 8% to 15%, whereas supraphysiologic concentrations (10(-9) to 10(-6) mol/L) increase transport by up to 60% (P < .05 v no increase over all concentrations tested). In SDa cells, insulin was more potent, displaying maximum transport stimulation of 70% at 10(-8) mol/L (P < .05 v a7r5 cells). Insulin regulation of glucose transport occurs by a protein synthesis-independent pathway as 10 mumol/L cycloheximide was without effect. Insulin produces these effects within 20 min of treatment, and cytochalasin B (10 mumol/L) inhibits both basal and insulin-stimulated glucose transport by 93% and 96%, respectively. Stimulation of insulin receptors alone, with 2.5 pg/mL insulin receptor-specific antibody, stimulates glucose transport by 20%, suggesting transport can be stimulated by an IGF-1 receptor independent mechanism. However, IGF-1 is a more potent stimulator of transport in both cell lines studied, with maximal stimulation (10(-8) mol/L IGF-1) of 60% and 80% in a7r5 and SDa cells, respectively (P < .05 v 10(-8) mol/L insulin in both cell lines). Insulin stimulation of glucose transport is specific for [D+]-glucose; [L-]-glucose does not compete for transport.(ABSTRACT TRUNCATED AT 250 WORDS)