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Myristic Acid Enhances Diacylglycerol Kinase delta-Dependent Glucose Uptake in Myotubes

机译:肉豆蔻酸增强肌管中的二酰基甘油激酶δ依赖性葡萄糖摄取。

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Decreased expression of diacylglycerol kinase (DGK) delta in skeletal muscles attenuates glucose uptake and is closely related to the pathogenesis of type 2 diabetes. Therefore, up-regulation of DGK delta expression is thought to protect and improve glucose homoeostasis in type 2 diabetes. We recently determined that myristic acid (14:0), but not palmitic (16:0) or stearic (18:0) acid, significantly increased DGK delta 2 protein expression in mouse C2C12 myotubes. In the current study, we analyzed whether myristic acid indeed enhances glucose uptake in C2C12 myotubes. We observed that myristic acid caused similar to 1.4-fold increase in insulin-independent glucose uptake. However, palmitic and stearic acids failed to enhance glucose uptake. DGK delta-specific siRNA decreased myristic acid-dependent increase of glucose uptake. Moreover, overexpression of DGK delta 2 enhanced glucose uptake in C2C12 cells in the absence of myristic acid treatment. Taken together, these results strongly suggest that myristic acid enhances basal glucose uptake in myotubes in a DGK delta 2 expression-dependent manner.
机译:骨骼肌中二酰基甘油激酶(DGK)δ的表达减少会减弱葡萄糖的摄取,并且与2型糖尿病的发病机理密切相关。因此,认为DGKδ表达的上调可保护和改善2型糖尿病的葡萄糖稳态。我们最近确定肉豆蔻酸(14:0),但不是棕榈酸(16:0)或硬脂酸(18:0),可显着增加小鼠C2C12肌管中DGK delta 2蛋白的表达。在当前的研究中,我们分析了肉豆蔻酸是否确实增强了C2C12肌管中的葡萄糖摄取。我们观察到肉豆蔻酸引起胰岛素非依赖性葡萄糖摄取增加约1.4倍。然而,棕榈酸和硬脂酸不能增强葡萄糖的摄取。 DGKδ特异性siRNA减少了肉豆蔻酸依赖性的葡萄糖摄取增加。此外,在没有肉豆蔻酸处理的情况下,DGK delta 2的过表达增强了C2C12细胞的葡萄糖摄取。综上所述,这些结果强烈暗示肉豆蔻酸以DGK delta 2表达依赖性方式增强肌管中的基础葡萄糖摄取。

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