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Activation of PKB and ERK, but not PI3K, is involved in fucosylated chondroitin sulphate from Acaudina molpadioides induced glucose uptake
- Hu, Shiwei, Xu, Hui, Chen, Ruixi, Wang, Jingfeng, Li, Zhaojie, Xu, Jiachao
- Journal of functional foods 2014 v.10 pp. 385-396
- Acaudina molpadioides, adipocytes, adipose tissue, blood glucose, chondroitin sulfate, glucose, glucose transporters, hyperglycemia, insulin resistance, mice, mitogen-activated protein kinase, phosphatidylinositol 3-kinase, phosphorylation
- Fucosylated chondroitin sulphate from sea cucumber can mitigate hyperglycaemia. However, the possible mechanism is unclear. We investigated the effects of fucosylated chondroitin sulphate from Acaudina molpadioides (Am-CHS) on glucose uptake and its mechanism using TNF-α-induced 3T3-L1 insulin resistant adipocytes. Results showed that Am-CHS could significantly increase glucose uptake and GLUT4 translocation, and phosphorylated PI3K, PKB, and ERK. Am-CHS reversed MK2206-induced reduction in glucose uptake, GLUT4 translocation, and PKB phosphorylation. Am-CHS antagonized U0126-induced decrease in glucose uptake, GLUT4 translocation, and ERK1/2 phosphorylation. Am-CHS inhibited wortmannin-induced reduction in glucose uptake and GLUT4 translocation reduction. Wortmannin-restrained PKB and ERK1/2 phosphorylation was antagonized by Am-CHS, but the lowered PI3K phosphorylation remained unchanged. Am-CHS also lowered blood glucose, increased m-GLUT4, p-PKB (Ser473), p-ERK1/2, p-PI3K p85, and p-IRS-1 (Tyr612) expressions, and decreased p-PKB (Ser308) expression in adipose tissues of insulin resistant mice. These indicate that PKB and ERK activation are involved in Am-CHS-triggered glucose, but not PI3K.