School of Food and Biological Engineering, Jiangsu University, Zhenjiang, Jiangsu, China.
School of the Environment and Safety Engineering, Jiangsu University, Zhenjiang, Jiangsu, China.
Indian J Pharmacol. 2020 Jan-Feb;52(1):31-38. doi: 10.4103/ijp.IJP_608_18. Epub 2020 Mar 11.
Our published literature indicated that chromium citrate could regulate the glycemic index in alloxaninduced diabetic mice. The present study investigated the mechanism of chromium citrate in insulin resistance (IR) buffalo rat liver (BRL) cells.
Chromium citrate was synthesized in our laboratory. BRL cells were purchased from the Chinese Academy of Sciences Cell Bank. The glucose transport and IR affected by chromium citrate in BRL cells were examined. The Thiazolyl Blue Tetrazolium Bromide (MTT) and glucose assay experiments were measured by microplate ELISA reader. The protein kinase B (Akt), glucose transporter-4 (Glut4), and phosphor-AMP-activated protein kinase β1 levels were tested by Western blot, and the mRNA expression of glucose transport proteins (Akt2, Glut4, and AMPactivated protein kinase α2 (AMPKα2)) and insulin sensitivity proteins (insulin receptor substrate1 (IRS-1), phosphatidylinositol 3 kinase (PI3K), and peroxisome proliferator-activated receptor γ (PPARγ)) was measured by reverse transcription-polymerase chain reaction.
The results indicated that the glucose absorption level of chromium citrate groups was higher than model group significantly. It demonstrated that chromium citrate could significantly improve glucose absorption in IR BRL cells. The Akt, Glut4, and phosphor-AMPKβ1 levels in chromium citrate groups (at doses of 0.4, 0.2, and 0.1 μg Cr/mL) were markedly improved when compared with the other experiment groups, and chromium citrate could more effectively increase the Akt level than chromium trichloride. In addition, the mRNA expression of Akt2, Glut4, and AMPKα2 in chromium citrate groups was significantly improved when contrasted with model group.
The consequences illustrated that chromium citrate can affect the IR BRL cells' ameliorating glucose transport and IR.
我们已发表的文献表明，柠檬铬可以调节四氧嘧啶诱导的糖尿病小鼠的血糖指数。本研究旨在探讨柠檬铬在胰岛素抵抗（IR）水牛大鼠肝（BRL）细胞中的作用机制。
我们实验室合成了柠檬铬。BRL 细胞购自中国科学院细胞库。检测了柠檬铬对 BRL 细胞葡萄糖转运和 IR 的影响。通过微孔板 ELISA 读取器测量噻唑蓝四唑溴盐（MTT）和葡萄糖测定实验。通过 Western blot 检测蛋白激酶 B（Akt）、葡萄糖转运蛋白-4（Glut4）和磷酸-AMP 激活蛋白激酶β1 的水平，并通过逆转录-聚合酶链反应测量葡萄糖转运蛋白（Akt2、Glut4 和 AMP 激活蛋白激酶α2（AMPKα2））和胰岛素敏感性蛋白（胰岛素受体底物 1（IRS-1）、磷脂酰肌醇 3 激酶（PI3K）和过氧化物酶体增殖物激活受体γ（PPARγ））的 mRNA 表达。
结果表明，柠檬铬组的葡萄糖吸收水平明显高于模型组，表明柠檬铬可显著改善 IR BRL 细胞的葡萄糖吸收。与其他实验组相比，柠檬铬组（0.4、0.2 和 0.1μg Cr/mL 剂量）的 Akt、Glut4 和磷酸-AMPKβ1 水平明显提高，且柠檬铬对 Akt 水平的提升作用优于三氯化铬。此外，与模型组相比，柠檬铬组的 Akt2、Glut4 和 AMPKα2 mRNA 表达明显改善。
结果表明，柠檬铬可影响 IR BRL 细胞改善葡萄糖转运和 IR。
