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白细胞介素-6及白细胞介素-6受体对小鼠骨骼肌葡萄糖转运的影响。

The effect of interleukin-6 and the interleukin-6 receptor on glucose transport in mouse skeletal muscle.

作者信息

Gray Stuart R, Ratkevicius Aivaras, Wackerhage Henning, Coats Paul, Nimmo Myra A

机构信息

Department of Sport & Exercise Sciences, Loughborough University, Ashby Road, Loughborough, Leicestershire LE113TU, UK.

出版信息

Exp Physiol. 2009 Aug;94(8):899-905. doi: 10.1113/expphysiol.2009.048173. Epub 2009 May 29.

DOI:10.1113/expphysiol.2009.048173
PMID:19482899
Abstract

Exercise results in an increase in interleukin-6 (IL-6), its receptor (IL-6R) and skeletal muscle glucose transport. Interleukin-6 has been found to have equivocal effects on glucose transport, with no studies, to our knowledge, investigating any potential role of IL-6R. In the present study, we hypothesized that a combined preparation of IL-6 and soluble IL-6R (sIL-6R) would stimulate glucose transport. Mouse soleus muscles were incubated with physiological and supraphysiological concentrations of IL-6 and a combination of IL-6 and sIL-6R. Total and phosphorylated AMP-activated protein kinase (AMPK) and Protein Kinase B (PKB/Akt) were also measured by Western blotting. Exposure to both physiological (80 pg ml(-1)) and supraphysiological IL-6 (120 ng ml(-1)) had no effect on glucose transport. At physiological levels, exposure to a combination of IL-6 and sIL-6R (32 ng ml(-1)) resulted in a 1.4-fold increase (P < 0.05) in basal glucose transport with no change to the phosphorylation of AMPK. Exposure to supraphysiological levels of IL-6 and sIL-6R (120 ng ml(-1)) resulted in an approximately twofold increase (P < 0.05) in basal glucose transport and an increase (P < 0.05) in AMPK phosphorylation. No effect of IL-6 or sIL-6R was observed on insulin-stimulated glucose transport. These findings demonstrate that, while IL-6 alone does not stimulate glucose transport in mouse soleus muscle, when sIL-6R is introduced glucose transport is directly stimulated, partly through AMPK-dependent signalling.

摘要

运动可导致白细胞介素-6(IL-6)、其受体(IL-6R)以及骨骼肌葡萄糖转运增加。白细胞介素-6对葡萄糖转运的影响一直存在争议,据我们所知,尚无研究探讨IL-6R的任何潜在作用。在本研究中,我们假设IL-6与可溶性IL-6R(sIL-6R)的联合制剂会刺激葡萄糖转运。将小鼠比目鱼肌与生理浓度和超生理浓度的IL-6以及IL-6与sIL-6R的组合一起孵育。还通过蛋白质印迹法测量了总AMP激活蛋白激酶(AMPK)和磷酸化AMP激活蛋白激酶以及蛋白激酶B(PKB/Akt)。暴露于生理浓度(80 pg/ml(-1))和超生理浓度的IL-6(120 ng/ml(-1))对葡萄糖转运均无影响。在生理水平下,暴露于IL-6与sIL-6R的组合(32 ng/ml(-1))会导致基础葡萄糖转运增加1.4倍(P<0.05),而AMPK的磷酸化没有变化。暴露于超生理水平的IL-6与sIL-6R(120 ng/ml(-1))会导致基础葡萄糖转运增加约两倍(P<0.05),并且AMPK磷酸化增加(P<0.05)。未观察到IL-6或sIL-6R对胰岛素刺激的葡萄糖转运有影响。这些发现表明,虽然单独的IL-6不会刺激小鼠比目鱼肌中的葡萄糖转运,但引入sIL-6R后会直接刺激葡萄糖转运,部分是通过AMPK依赖性信号传导实现的。

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