陈欣,刘双,文琴,王越,邓杰文,凌宏艳,奉水东.二氢杨梅素通过抑制骨骼肌TCPTP改善2型糖尿病大鼠胰岛素抵抗.[J].中南医学科学杂志.,2022,(1):55-58.
二氢杨梅素通过抑制骨骼肌TCPTP改善2型糖尿病大鼠胰岛素抵抗
Dihydromyricetin improves insulin resistance in type 2 diabetic rats by inhibiting TCPTP in skeletal muscle
投稿时间:2021-05-19  修订日期:2021-07-06
DOI:10.15972/j.cnki.43-1509/r.2022.01.012
中文关键词:  二氢杨梅素  2型糖尿病  骨骼肌TCPTP  胰岛素抵抗
英文关键词:dihydromyricetin  type 2 diabetes mellitus  skeletal muscle TCPTP  insulin resistance
基金项目:湖南省自然科学基金(2021JJ30595);湖南省大学生创新创业训练计划项目(X2019195) 作者简介:陈欣,E-mail为1106460924@qq.com。通信作者凌宏艳,博士,教授,硕士研究生导师,研究方向为2型糖尿病发病机制及防冶,E-mail为linghongyan0203@126.com。奉水东,博士,副教授,硕士研究生导师,研究方向为糖尿病流行病学研究,E-mail为shuidong_f@hotmail.com。
作者单位E-mail
陈欣 南华大学衡阳医学院公共卫生学院,湖南省衡阳市 421001  
刘双 南华大学衡阳医学院公共卫生学院,湖南省衡阳市 421001  
文琴 南华大学衡阳医学院公共卫生学院,湖南省衡阳市 421001  
王越 南华大学衡阳医学院公共卫生学院,湖南省衡阳市 421001  
邓杰文 南华大学衡阳医学院公共卫生学院,湖南省衡阳市 421001  
凌宏艳 南华大学衡阳医学院基础医学院生理学教研室,湖南省衡阳市 421001 e-mail为1106460924@qq.com,e-mail为linghongyan0203@126.com,e-mail为shuidong_f@hotmail.com 
奉水东 南华大学衡阳医学院公共卫生学院,湖南省衡阳市 421001 e-mail为1106460924@qq.com,e-mail为linghongyan0203@126.com,e-mail为shuidong_f@hotmail.com 
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中文摘要:
      目的观察二氢杨梅素(DMY)对2型糖尿病(T2DM)大鼠胰岛素抵抗的影响。方法将SD雄性大鼠随机分成正常对照组、2型糖尿病组、2型糖尿病DMY组、DMY对照组。高糖高脂饮食联合链脲佐菌素造模。16周末,大鼠称重后测定空腹血糖(FBG)和血胰岛素(FINS),计算胰岛素敏感指数(ISI),Western blot检测大鼠骨骼肌T细胞蛋白酪氨酸磷酸酶(TCPTP)、蛋白质丝氨酸苏氨酸激酶(Akt)及磷酸化蛋白质丝氨酸苏氨酸激酶(p-Akt)、磷脂酰肌醇3-激酶(PI3K)及磷酸化磷脂酰肌醇3-激酶(p-PI3K)、葡萄糖转运蛋白4(GLUT4)的表达。结果成功建立2型糖尿病大鼠模型。与正常对照组比较,2型糖尿病组大鼠体质量、ISI及p-Akt、p-PI3K、GLUT4的表达水平显著降低,FBG、FINS及TCPTP表达水平显著升高(P<0.05);与2型糖尿病组比较,2型糖尿病DMY组大鼠体质量、ISI及p-Akt、p-PI3K、GLUT4的表达水平显著升高,FBG、FINS及TCPTP表达水平显著降低(P<0.05),DMY对正常大鼠上述指标无显著影响。结论二氢杨梅素可能通过抑制骨骼肌TCPTP的表达从而改善2型糖尿病大鼠胰岛素抵抗。
英文摘要:
      To observe the effect of dihydromyricetin (DMY) on insulin resistance in type 2 diabetes mellitus (T2DM) rats. MethodsSD rats were randomly divided into normal control group, type 2 diabetes group, type 2 diabetes DMY group, DMY control group. Model rats were made by by high glucose and high fat diet combined with streptozocin. At the end of 16 weeks, fasting blood glucose (FBG) and fasting insulin (FINS) were measured, and insulin sensitivity index (ISI) was calculated. Protein expressions of protein tyrosine phosphatase (TCPTP), protein serine threonine kinase(Akt), phosphorylated protein serine threonine kinase (p-Akt), phosphatidylinositol 3-kinase (PI3K), phosphorylated phosphatidylinositol 3-kinase (p-PI3K) and glucose transporter 4 (GLUT4) were detected by Western blot.ResultsT2DM rat model was successfully established. Compared with the control group, the body weight, ISI and the expression levels of P-Akt and p-PI3K, GLUT4 in T2DM group were significantly decreased, while the expression levels of FBG, FINS and TCPTP were significantly increased; Compared with type 2 diabetic group, body weight, ISI, P-Akt, P-PI3K and GLUT4 expression levels were significantly increased in TYPE 2 diabetic DMY group, while FBG, FINS and TCPTP expression levels were significantly decreased (P<0.05). DMY has no significant effect on the above indexes in normal rats. ConclusionDMY may improve insulin resistance in T2DM rats by inhibiting the expression of TCPTP in skeletal muscle.
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