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首页> 外文期刊>Journal of Physiology and Biochemistry >Ursolic acid and rosiglitazone combination improves insulin sensitivity by increasing the skeletal muscle insulin-stimulated IRS-1 tyrosine phosphorylation in high-fat diet-fed C57BL/6J mice
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Ursolic acid and rosiglitazone combination improves insulin sensitivity by increasing the skeletal muscle insulin-stimulated IRS-1 tyrosine phosphorylation in high-fat diet-fed C57BL/6J mice

机译：乌索酸和罗格列酮组合可通过增加高脂饮食喂养的C57BL / 6J小鼠的骨骼肌胰岛素刺激的IRS-1酪氨酸磷酸化来改善胰岛素敏感性

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The aim of this present study was to investigate the effect of ursolic acid (UA) and rosiglitazone (RSG) on insulin sensitivity and proximal insulin signaling pathways in high-fat diet (HFD)-fed C57/BL/6J mice. Male C57BL/6J mice were fed either normal diet or HFD for 10 weeks, after which animals in each dietary group were divided into the following six groups (normal diet, normal diet plus UA and RSG, HFD alone, HFD plus UA, HFD plus RSG, and HFD plus UA and RSG) for the next 5 weeks. UA (5 mg/kg BW) and RSG (4 mg/kg BW) were administered as suspensions directly into the stomach using a gastric tube. The HFD diet elevated fasting plasma glucose, insulin, and homeostasis model assessment index. The expression of insulin receptor substrate (IRS)-1, phosphoinositide 3-kinase (PI3-kinase), Akt, and glucose transporter (GLUT) 4 were determined by Western blot analyses. The results demonstrated that combination treatment (UA/RSG) ameliorated HFD-induced glucose intolerance and insulin resistance by improving the homeostatic model assessment (HOMA) index. Further, combination treatment (UA/RSG) stimulated the IRS-1, PI3-kinase, Akt, and GLUT 4 translocation. These results strongly suggest that combination treatment (UA/RSG) activates IRS-PI3-kinase-Akt-dependent signaling pathways to induce GLUT 4 translocation and increases the expression of insulin receptor to improve glucose intolerance.
机译：本研究的目的是研究熊果酸（UA）和罗格列酮（RSG）对高脂饮食（HFD）喂养的C57 / BL / 6J小鼠胰岛素敏感性和近端胰岛素信号通路的影响。给雄性C57BL / 6J小鼠喂食正常饮食或HFD 10周，然后将每个饮食组的动物分为以下六组（正常饮食，正常饮食加UA和RSG，仅HFD，HFD加UA，HFD加RSG，HFD以及UA和RSG）在接下来的5周内。 UA（5 mg / kg BW）和RSG（4 mg / kg BW）以悬浮液的形式通过胃管直接注入胃中。 HFD饮食可提高空腹血糖，胰岛素和体内稳态模型评估指标。通过Western印迹分析确定胰岛素受体底物（IRS）-1，磷酸肌醇3-激酶（PI3-激酶），Akt和葡萄糖转运蛋白（GLUT）4的表达。结果表明，联合治疗（UA / RSG）通过改善稳态模型评估（HOMA）指数改善了HFD诱导的葡萄糖耐量和胰岛素抵抗。此外，联合治疗（UA / RSG）刺激了IRS-1，PI3-激酶，Akt和GLUT 4易位。这些结果强烈表明联合治疗（UA / RSG）激活IRS-PI3-激酶-Akt依赖性信号传导途径，以诱导GLUT 4易位，并增加胰岛素受体的表达，从而改善葡萄糖耐量。

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