过剩4
胰岛素抵抗
脂滴包被蛋白
油红O
化学
脂肪细胞
脂肪组织
内分泌学
内科学
活力测定
葡萄糖摄取
脂滴
葡萄糖转运蛋白
免疫印迹
胰岛素
蛋白激酶B
PI3K/AKT/mTOR通路
脂肪生成
细胞
生物化学
细胞凋亡
生物
医学
基因
作者
Changqin Cheng,Zhiyong Li,Min Zhang,Dezhi Chen
标识
DOI:10.1080/10799893.2020.1806319
摘要
Jateorhizine (Jat) can reduce blood glucose in diabetic mice, but there are few studies on its role in insulin resistance (IR). This study analyzed the effect of Jat on adipocytes, so as to provide an evidence for the clinical application of Jat. MDI was used to differentiate preadipocytes into adipocytes and induce IR cell models. Different concentrations of Jat (1, 5, 10, 20 μmol/L) were added into undifferentiated and differentiated cells. The cell viability was detected using MTT method. Oil red O staining was performed to observe the lipid formation in cells. Adipolysis method was used to detect the release of glycerol in cell culture medium. The level of 2-DG in cells was detected by glucose uptake assay based on insulin treatment. The expression of adipose transcription factors and IRS2/p-PI3K/p-AKT/GLUT4 signaling pathway was analyzed by western blot (WB) analysis. Neither the activity of differentiated nor undifferentiated preadipocytes was affected by the addition of Jat. There was numerous lipid formation in cells induced by MDI, which was decreased visibly by Jat. Jat reduced the expression levels of MDI-induced elevated levels of PPARγ, C/EBPα, FABP4, perilipin and FAS, as well as increased the release of glycerol in adipocytes. Moreover, Jat further enhanced the 2-DG uptake in MDI-induced adipocytes, and activated the IRS2/p-PI3K/p-AKT/GLUT4 signaling pathway. In general, the role of Jat in adipocytes was concentration-dependent. Jat can not only promote adipolysis, but also increase the glucose uptake in adipocytes, which might be a potential therapy for IR.
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