Choi Kyeong-Mi, Kim Wonkyun, Hong Jin Tae, Yoo Hwan-Soo
College of Pharmacy, Chungbuk National University, 1 Chungdae-ro, Seowon-Gu, Cheongju, 28644, Republic of Korea.
Mol Cell Biochem. 2017 Feb;426(1-2):9-15. doi: 10.1007/s11010-016-2876-x. Epub 2016 Nov 16.
Dodeca-2(E),4(E)-dienoic acid isobutylamide (DDI), an alkamide derived from the plant Echinacea purpurea, promotes adipocyte differentiation and activates peroxisome proliferator-activated receptor γ, which is associated with enhanced insulin sensitivity. In the present study, we investigated whether DDI may increase glucose uptake through activation of the insulin signaling pathway in 3T3-L1 adipocytes. DDI increased insulin-stimulated glucose uptake, and expression and translocation of glucose transporter 4 in adipocytes treated with sub-optimal levels of insulin. Additionally, DDI enhanced Akt phosphorylation, whereas phosphoinositide 3-kinase/Akt inhibitors suppressed DDI-induced glucose uptake. These results suggest that DDI may improve insulin sensitivity through the activation of Akt signaling, which leads to enhanced glucose uptake.
紫锥菊酰胺（DDI）是一种从紫锥菊中提取的链状酰胺，可促进脂肪细胞分化并激活过氧化物酶体增殖物激活受体γ，这与增强胰岛素敏感性有关。在本研究中，我们探究了DDI是否可通过激活3T3-L1脂肪细胞中的胰岛素信号通路来增加葡萄糖摄取。DDI增加了胰岛素刺激的葡萄糖摄取，以及在次优胰岛素水平处理的脂肪细胞中葡萄糖转运蛋白4的表达和转位。此外，DDI增强了Akt磷酸化，而磷酸肌醇3激酶/Akt抑制剂抑制了DDI诱导的葡萄糖摄取。这些结果表明，DDI可能通过激活Akt信号通路来改善胰岛素敏感性，从而增强葡萄糖摄取。
