Adiponectin is a fat-derived cytokine with anti-diabetic and anti-atherogenic properties. In this study, effects of sulfonylureas (SUs) on adiponectin production and the action mechanism were evaluated using 3T3-L1 adipocytes. The cells were incubated with glimepiride, glibenclamide, gliclazide, pioglitazone, metformin and the medium only as the control. In the control, the adiponectin level evaluated as the production rate per 24 h was not changed, while pioglitazone significantly increased the adiponectin level. SUs also increased the adiponectin level, but metformin failed to show any increase in adiponectin production. SUs induced adiponectin gene expression as well as pioglitazone. Pioglitazone significantly increased adipogenesis, but glimepiride did not. The aP2 gene expression was increased by pioglitazone, but not by glimepiride. Forskolin, a protein kinase A stimulator, reduced the adiponectin production stimulated by glimepiride but not by pioglitazone. These observations strongly suggest that SUs stimulate the adiponectin production through a different mechanism from pioglitazone, namely an interaction with protein kinase A activity. The significance of the extrapancreatic action of SUs observed in this study should be further evaluated in the clinical field.

译文

脂联素是一种具有抗糖尿病和抗动脉粥样硬化特性的脂肪衍生细胞因子。在这项研究中,使用3T3-L1脂肪细胞评估了磺脲类 (SUs) 对脂联素产生的影响及其作用机制。将细胞与格列美脲,格列本脲,格列齐特,吡格列酮,二甲双胍和仅作为对照的培养基孵育。在对照中,评估为每24小时产生速率的脂联素水平没有改变,而吡格列酮显着增加了脂联素水平。SUs也增加了脂联素水平,但二甲双胍未能显示出脂联素产生的任何增加。SUs诱导脂联素基因表达以及吡格列酮。吡格列酮显着增加脂肪生成,但格列美脲没有。吡格列酮增加了aP2基因的表达,但格列美脲没有增加。Forskolin是一种蛋白激酶a刺激剂,可减少格列美脲但吡格列酮刺激的脂联素产生。这些观察结果强烈表明,SUs通过与吡格列酮不同的机制刺激脂联素的产生,即与蛋白激酶a活性的相互作用。在本研究中观察到的SUs胰腺外作用的重要性应在临床领域进一步评估。

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