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苹果酸铬通过葡萄糖摄取和胰岛素敏感性信号通路改善3T3-L1脂肪细胞的高糖和胰岛素抵抗及其机制

Improvement of high-glucose and insulin resistance of chromium malate in 3T3-L1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism.

作者信息

Feng Weiwei, Liu Yongchao, Fei Fan, Chen Yao, Ding Yangyang, Yan Mengjiao, Feng Yun, Zhao Ting, Mao Guanghua, Yang Liuqing, Wu Xiangyang

机构信息

Institute of Environmental Health and Ecological Security, School of the Environment and Safety Engineering, Jiangsu University 301 Xuefu Rd. 212013 Zhenjiang Jiangsu China

School of Medical Science and Laboratory Medicine, Jiangsu University 301 Xuefu Rd. 212013 Zhenjiang Jiangsu China.

出版信息

RSC Adv. 2018 Dec 21;9(1):114-127. doi: 10.1039/c8ra07470d. eCollection 2018 Dec 19.

DOI:10.1039/c8ra07470d
PMID:35521592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9059288/
Abstract

Previous study has revealed that chromium malate could improve insulin resistance and the regulation of fasting blood glucose in type 2 diabetic rats. This study was designed to investigate the effect of chromium malate on hypoglycemic and improve insulin resistance activities in 3T3-L1 adipocytes with insulin resistance and investigate the acting mechanism. The result indicated that chromium malate exhibited direct hypoglycemic activity . Compared with the model group, chromium malate could significantly promote the expression levels of GLUT-4, Akt, Irs-1, PPARγ, PI3K and p38-MAPK and their mRNA, increase -AKT/AKT level, AKT and AMPKβ1 phosphorylation and reduce Irs-1 phosphorylation and -Irs-1/Irs-1 level in 3T3-L1 adipocytes ( < 0.05). Chromium malate is more effective in regulating the proteins and mRNA expressions than those of chromium trichloride and chromium picolinate. Compared to the model group, pretreatment with the specific p38-MAPK inhibitor completely inhibited the GLUT-4 and Irs-1 proteins and mRNA expressions induced by the chromium malate. In conclusion, chromium malate had a beneficial influence on improvement of controlling glucose levels and insulin resistance in 3T3-L1 adipocytes with insulin resistance by regulating proteins productions and genes expressions in glucose uptake and insulin sensitivity signaling pathways.

摘要

先前的研究表明,苹果酸铬可改善2型糖尿病大鼠的胰岛素抵抗及空腹血糖调节。本研究旨在探讨苹果酸铬对胰岛素抵抗的3T3-L1脂肪细胞的降糖及改善胰岛素抵抗活性的作用,并研究其作用机制。结果表明,苹果酸铬具有直接降糖活性。与模型组相比,苹果酸铬可显著促进3T3-L1脂肪细胞中GLUT-4、Akt、Irs-1、PPARγ、PI3K和p38-MAPK及其mRNA的表达水平,增加-AKT/AKT水平、AKT和AMPKβ1磷酸化水平,并降低Irs-1磷酸化水平和-Irs-1/Irs-1水平(P<0.05)。苹果酸铬在调节蛋白质和mRNA表达方面比三氯化铬和吡啶甲酸铬更有效。与模型组相比,用特异性p38-MAPK抑制剂预处理可完全抑制苹果酸铬诱导的GLUT-4和Irs-1蛋白及mRNA表达。总之,苹果酸铬通过调节葡萄糖摄取和胰岛素敏感性信号通路中的蛋白质生成和基因表达,对改善胰岛素抵抗的3T3-L1脂肪细胞的血糖控制和胰岛素抵抗具有有益影响。

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