We aim to investigate the expression of the glucagon receptor (GCGR) in human adipose tissue, and the impact of glucagon in glucose uptake and lipolysis in human adipocytes. GCGR gene expression in human subcutaneous and visceral adipose tissue was demonstrated, albeit at low levels and with an inter-individual variation. Furthermore, GCGR expression was not significantly different between subjects with T2D and matched controls, and we found no significant association with BMI. Glucagon only at a supra-physiological concentration (10-100 nM) significantly increased basal and insulin-stimulated glucose uptake by up to 1.5-fold. Also, glucagon (0.01 and 1 nM) dose-dependently increased basal and isoproterenol-stimulated lipolysis up to 3.7- and 1.7-fold, respectively, compared to control. In addition, glucagon did not change insulin sensitivity to stimulate glucose uptake or inhibit lipolysis. In conclusion, we show that the GCGR gene is expressed at low levels in human adipose tissue, and glucagon at high concentrations can increase both glucose uptake and lipolysis in human adipocytes. Taken together, our data suggest that glucagon at physiological levels has minor direct effects on the regulation of adipocyte metabolism, but does not antagonize the insulin effect to stimulate glucose uptake and inhibit lipolysis in human adipocytes.

中文翻译：

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胰高血糖素对人脂肪细胞中葡萄糖摄取和脂解的直接作用。

我们旨在研究胰高血糖素受体（GCGR）在人脂肪组织中的表达，以及胰高血糖素对人脂肪细胞中葡萄糖摄取和脂解的影响。证实了人皮下和内脏脂肪组织中的GCGR基因表达，尽管其水平较低且个体间存在差异。此外，在患有T2D的受试者和匹配的对照之间，GCGR表达没有显着差异，并且我们发现与BMI没有显着相关性。仅在超生理浓度（10-100 nM）的胰高血糖素显着增加基础和胰岛素刺激的葡萄糖摄取，最多可增加1.5倍。同样，与对照相比，胰高血糖素（0.01和1 nM）剂量依赖性地增加了基础和异丙肾上腺素刺激的脂解，分别高达3.7和1.7倍。此外，胰高血糖素没有改变胰岛素敏感性以刺激葡萄糖摄取或抑制脂解。总之，我们表明，GCGR基因在人的脂肪组织中低水平表达，而高浓度的胰高血糖素可增加人脂肪细胞中的葡萄糖摄取和脂解作用。两者合计，我们的数据表明，在生理水平上的胰高血糖素对脂肪细胞代谢的调节具有较小的直接影响，但不会拮抗胰岛素的作用以刺激人体脂肪细胞中的葡萄糖摄取和抑制脂解作用。