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Fucoxanthin promotes translocation and induction of glucose transporter 4 in skeletal muscles of diabetic/obese KK-A y mice

机译:岩藻黄质促进糖尿病/肥胖KK-A y小鼠骨骼肌中葡萄糖转运蛋白4的转运和诱导

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摘要

Fucoxanthin (Fx) isolated from Undaria pinnatifida suppresses the development of hyperglycemia and hyperinsulinemia of diabetic/obese KK-A y mice after 2 weeks of feeding 0.2% Fx-containing diet. In the soleus muscle of KK-A y mice that were fed Fx, glucose transporter 4 (GLUT4) translocation to plasma membranes from cytosol was promoted. On the other hand, Fx increased GLUT4 expression levels in the extensor digitorum longus (EDL) muscle, although GLUT4 translocation tended to increase. The expression levels of insulin receptor (IR) mRNA and phosphorylation of Akt, which are in upstream of the insulin signaling pathway regulating GLUT4 translocation, were also enhanced in the soleus and EDL muscles of the mice fed Fx. Furthermore, Fx induced peroxisome proliferator activated receptor γ coactivator-1α (PGC-1α), which has been reported to increase GLUT4 expression, in both soleus and EDL muscles. These results suggest that in diabetic/obese KK-A y mice, Fx improves hyperglycemia by activating the insulin signaling pathway, including GLUT4 translocation, and inducing GLUT4 expression in the soleus and EDL muscles, respectively, of diabetic/obese KK-A y mice.
机译:饲喂含0.2%Fx的饲料2周后,从裙带菜中分离出的岩藻黄质(Fx)抑制了糖尿病/肥胖KK-A y小鼠的高血糖和高胰岛素血症。在喂Fx的KK-A y小鼠的比目鱼肌中,促进了葡萄糖转运蛋白4(GLUT4)从胞质溶胶转移到质膜。另一方面,尽管GLUT4易位性增加,但Fx增加了趾长伸肌(EDL)肌肉中GLUT4的表达水平。 Fx小鼠的比目鱼肌和EDL肌肉中,在调节GLUT4易位的胰岛素信号通路上游,胰岛素受体(IR)mRNA的表达水平和Akt的磷酸化也得到了增强。此外,据报道,Fx诱导了过氧化物酶体增殖物激活的受体γ共激活因子1α(PGC-1α)在比目鱼肌和EDL肌肉中均能增加GLUT4的表达。这些结果表明,在糖尿病/肥胖KK-A y小鼠中,Fx通过激活胰岛素信号通路(包括GLUT4易位)并分别诱导糖尿病/肥胖KK-A y小鼠的比目鱼肌和EDL肌肉中GLUT4表达来改善高血糖症。 。

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