克仑特罗刺激的葡萄糖摄取通过Β2-Adrenoceptor激活小鼠离体比目鱼肌的GS和GI通路

R. Ngala, J. Arch, M. Cawthorne
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引用次数: 0

摘要

由肾上腺素激活的β2-肾上腺素受体也可以与g蛋白和Gi蛋白偶联。前者与cAMP的增加有关,从而使儿茶酚胺的作用失效。在后者中,β2-AR诱导pka催化的受体磷酸化,并在高浓度下与Gi偶联。我们提出,低浓度刺激葡萄糖摄取,高浓度抑制葡萄糖摄取的克仑特罗可能与肾上腺素具有相同的信号通路。小鼠离体肌肉在含有3ml Krebs-Henseleit碳酸氢钠缓冲液的烧瓶中预孵育。预孵育120分钟后,用适当浓度的PTX将肌肉转移到另一个孵育瓶中,该孵育瓶中含有3ml相同的缓冲液和0.3mCi 2-脱氧[1-14C]葡萄糖,其中含有不同浓度的肾上腺素、克伦特罗或1nM胰岛素,其中PTX浓度为肾上腺素和克伦特罗100ng/ml,胰岛素0.1或1.0ng/ml,或1M乙酰胆碱,孵育45分钟。肾上腺素在低浓度(10-10M)刺激离体小鼠比目鱼肌对葡萄糖的摄取,在高浓度(10-5M)抑制其摄取。低浓度的作用是通过β2-AR与Gs蛋白和高浓度的Gi蛋白偶联介导的。同样,低浓度(10-11M)的克仑特罗刺激葡萄糖摄取是通过β2-AR偶联到Gs蛋白和高浓度(10-7M)的Gi蛋白介导的。100ng/ml PTX可减轻肾上腺素和盐酸克仑特罗的抑制作用。盐酸克仑特罗具有较高的浓度效应,另外,1M的乙酰胆碱也减轻了抑制作用。关键词:PTX,百日咳毒素,g蛋白,鸟嘌呤核苷酸结合蛋白,β-AR, β肾上腺素受体,M2,毒蕈碱受体
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Clenbuterol-Stimulated Glucose Uptake Activates both GS and GI Pathways through Β2-Adrenoceptor in Mouse Isolated Soleus Muscle
β2-adrenoceptors activated by adrenaline can also couple to both Gs and Gi proteins. The former is associated with an increase in cAMP to illicit the effect of the catecholamine. In the later, β2-AR induces PKA-catalysed phosphorylation of the receptor, which intends couples to Gi, at high concentration. We proposed that, clenbuterol which stimulates glucose uptake at low concentra-tion and inhibits it at high concentration might have identical signalling pathway as adrenaline. Mouse isolated muscles were pre-incubated in flasks containing 3 ml of Krebs-Henseleit Bicar-bonate buffer. After 120 min of pre-incubation, with the appropriate concentration of PTX the muscles were transferred to another incubation flask containing 3 ml of the same buffer and 0.3mCi 2-deoxy[1-14C]glucose containing varying concentrations of adrenaline, clenbuterol or 1nM insulin with or without PTX concentrations of 100ng/ml for adrenaline and clenbuterol and 0.1 or 1.0ng/ml for insulin, or 1M acetylcholine for 45 minutes. Adrenaline stimulated glu-cose uptake in isolated mouse soleus muscle at low concentration (10-10M) and inhibited it at high concentration (10-5M). The effect of the lower concentration was mediated through the β2-AR coupling to the Gs protein and to the Gi protein at high concentration. Similarly, clenbuterol stimulated glucose uptake at lower concentration (10-11M) is mediated through the β2-AR cou-pling to the Gs protein and to the Gi protein at the higher concentration (10-7M). These effects of high concentration of adrenaline and clenbuterol were supported by the fact that 100ng/ml PTX relieved their inhibitory effects. The higher concentration effect of clenbuterol was additionally supported by the fact that, 1M acetylcholine, relieved the inhibitory effect. Keywords: PTX, Pertusis toxin, G-proteins, Guanine nucleotide binding proteins, β-AR, beta adrenoceptor, M2, muscarinic receptors
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