The dietary intake of elaidate (elaidic acid), a trans-fatty acid, is associated with the development of various diseases. Since elaidate is a C18 unsaturated fatty acid with a steric structure similar to that of a C18 saturated fatty acid (stearate), we previously revealed that insulin-dependent glucose uptake was impaired in adipocytes exposed to elaidate prior to and during differentiation similar to stearate. However, it is still unknown whether the mechanism of impairment of insulin-dependent glucose uptake due to elaidate is similar to that of stearate. Here, we indicate that persistent exposure to elaidate has particular effects on insulin signaling and GLUT4 dynamics. Insulin-induced accumulation of Akt at the plasma membrane (PM) and elevations of phosphorylated Akt and AS160 levels in whole cells were suppressed in adipocytes persistently exposed to 50 μM elaidate. Interestingly, persistent exposure to the same concentration of stearate has no effect on the phosphorylated Akt and AS160 levels. When cells were exposed to these fatty acids, elaidate suppressed insulin-induced fusion, but not translocation, of GLUT4 storage vesicles in the PM, whereas stearate did not suppress the fusion and translocation of GLUT4 storage, indicating that elaidate has suppressive effects on the accumulation of Akt and fusion of GLUT4 storage vesicles and that both elaidate and stearate vary in the mechanisms by which they impair insulin-dependent glucose uptake.

饮食中反式脂肪酸乌来酸（花生酸）的摄入与多种疾病的发展有关。由于残留物是具有类似于C18饱和脂肪酸（硬脂酸酯）的空间结构的C18不饱和脂肪酸，因此我们先前揭示了在分化前和分化过程中与硬脂酸相似的脂肪细胞中，胰岛素依赖性葡萄糖的摄取受到损害。但是，尚不清楚由于隐伏酸酯引起的胰岛素依赖性葡萄糖摄取受损的机制是否与硬脂酸酯相似。在这里，我们表明持续暴露于残留物中对胰岛素信号传导和GLUT4动力学有特殊影响。在持续暴露于50μM残留物中的脂肪细胞中，胰岛素诱导的Akt在质膜（PM）的积累以及全细胞中磷酸化Akt和AS160水平的升高受到抑制。有趣的是，持续暴露于相同浓度的硬脂酸酯对磷酸化的Akt和AS160水平没有影响。当细胞暴露于这些脂肪酸时，残留物抑制胰岛素诱导的PM中GLUT4储存小泡的融合，但不抑制其易位，而硬脂酸酯则不能抑制GLUT4储存的融合和易位，这表明残留物对积累具有抑制作用。 Akt和GLUT4储存囊泡的融合以及卵磷脂和硬脂酸酯的受损在其依赖胰岛素​​依赖的葡萄糖摄取的机制上各不相同。持续暴露于相同浓度的硬脂酸酯对磷酸化的Akt和AS160水平没有影响。当细胞暴露于这些脂肪酸时，残留物抑制胰岛素诱导的PM中GLUT4储存小泡的融合，但不抑制其易位，而硬脂酸酯则不能抑制GLUT4储存的融合和易位，这表明残留物对积累具有抑制作用。 Akt和GLUT4储存囊泡的融合以及卵磷脂和硬脂酸酯的受损在其依赖胰岛素​​依赖的葡萄糖摄取的机制上各不相同。持续暴露于相同浓度的硬脂酸酯对磷酸化的Akt和AS160水平没有影响。当细胞暴露于这些脂肪酸时，残留物抑制胰岛素诱导的PM中GLUT4储存小泡的融合，但不抑制其易位，而硬脂酸酯则不能抑制GLUT4储存的融合和易位，这表明残留物对积累具有抑制作用。 Akt和GLUT4储存囊泡的融合以及卵磷脂和硬脂酸酯的受损在其依赖胰岛素​​依赖的葡萄糖摄取的机制上各不相同。