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首页> 外文期刊>Acta Physiologica Hungarica: A Periodical of the Hungarian Academy of Sciences >Rat white adipocytes activate p85/p110 PI3K and induce PM GLUT4 in response to adrenoceptor agonists or aluminum fluoride
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Rat white adipocytes activate p85/p110 PI3K and induce PM GLUT4 in response to adrenoceptor agonists or aluminum fluoride

机译:大鼠白色脂肪细胞激活p85 / p110 PI3K并诱导PM GLUT4,以响应肾上腺素受体激动剂或氟化铝

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摘要

Adipocyte responses to adrenergic and beta-adrenoceptor(-AR) (adrenoceptor) regulation are not sufficiently understood, and information helpful for elucidating the adrenoceptor-responsive machinery is insufficient. Here we show by using immunoprecipitated kinase analysis with a phosphatidylinositol 3-kinase (PI3K) p85 antibody that PI3K activation was induced by treatment with 10 or 100 mu M norepinephrine (NE) for 15 min or with 10 mM aluminum fluoride (AF, a guanosine triphosphate (GTP)-binding (G) protein activator) for 20 min in white adipocytes (rat epididymal adipocytes) and that treatment with pertussis toxin (PTX, a G-protein inactivator) inhibited PI3K activation induced by the 20-min treatment with AF in the cells. In addition, western blot analysis revealed that glucose transporter 4 (GLUT4) level in the adipocyte plasma membrane (PM) fraction was increased by treatment with 10 mu M NE, 100 mu M dobutamine (DOB, a beta(1)-AR agonist), or 0.1 mu M CL316243 (CL, a beta(3)-AR agonist) for 30 min or with 10 mM AF for 20 min. NE or AF treatment triggered 2-deoxyglucose (2-DG) uptake into adipocytes under the above conditions. Our results advance the understanding of responses to adrenoceptor regulation in white adipocytes and provide possible clues for clarifying the machinery involved in adrenergic and beta-AR responses in the cells.
机译:脂肪细胞对肾上腺素能和β-肾上腺素能受体(-AR)(肾上腺素能受体)调节的反应还不够充分,并且有助于阐明肾上腺素能反应机制的信息不足。在这里,我们通过使用磷脂酰肌醇3-激酶(PI3K)p85抗体进行的免疫沉淀激酶分析表明,通过用10或100μM去甲肾上腺素(NE)处理15分钟或用10 mM氟化铝(AF,鸟苷)处理可诱导PI3K激活。三磷酸(GTP)-结合(G)蛋白激活剂在白色脂肪细胞(大鼠附睾脂肪细胞)中作用20分钟,用百日咳毒素治疗(PTX,一种G蛋白灭活剂)抑制了AF 20分钟治疗诱导的PI3K激活在细胞中。此外,蛋白质印迹分析表明,通过用10μMNE,100μM多巴酚丁胺(DOB,β(1)-AR激动剂)处理,脂肪细胞质膜(PM)组分中的葡萄糖转运蛋白4(GLUT4)水平增加。 ,或0.1μM CL316243(CL,β(3)-AR激动剂)持续30分钟或用10 mM AF持续20分钟。在上述条件下,NE或AF处理触发了2-脱氧葡萄糖(2-DG)吸收进入脂肪细胞。我们的结果提高了对白色脂肪细胞中对肾上腺素受体调节反应的理解,并为阐明细胞中肾上腺素能和β-AR应答所涉及的机制提供了可能的线索。

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