二甲双胍对2型糖尿病模型大鼠胰岛素抵抗的影响

被引:12
作者
秦凤 [1 ]
李春亮 [2 ]
张惠莉 [1 ]
机构
[1] 青海大学附属医院内分泌科
[2] 青海大学医学院
关键词
糖尿病,2型; 二甲双胍; 胰岛素; 组织工程; 组织构建; 2型糖尿病; 胰岛素抵抗; 机制;
D O I
暂无
中图分类号
R587.1 [糖尿病]; R-332 [医用实验动物学];
学科分类号
摘要
背景:目前已经发现的脂肪代谢相关基因有10余种,脂肪代谢相关基因介导的内分泌功能失常是导致胰岛素抵抗发生、发展的重要病理基础。目的:分析二甲双胍对2型糖尿病大鼠血脂水平、胰岛素抵抗相关基因及肝脏和胰腺组织病理学变化的影响。方法:通过4周高脂饮食结合腹腔注射链脲佐菌素(35 mg/kg)建立2型糖尿病大鼠模型。4周高脂饮食时,模型大鼠同时口服二甲双胍4周[400 mg/(kg·d)],对照组大鼠正常饮食,腹腔未注射链脲佐菌素。然后利用半定量RT-PCR、组织病理学及生化检测等方法进行相关分析。结果与结论:(1)二甲双胍通过恢复2型糖尿病大鼠正常血脂,改善胰岛素抵抗症状;(2)二甲双胍上调脂肪代谢相关胰岛素受体和基因乙酰辅酶A氧化酶,肉毒碱棕榈酰转移1和过氧化物酶体增殖物激活受体α;(3)二甲双胍治疗下调胎球蛋白A和视黄醇结合蛋白,2型糖尿病大鼠中降低的脂滴包被蛋白也恢复正常;(4)在胰腺内,二甲双胍处理诱导胰岛素分泌和胰腺β细胞再生;(5)结果说明,二甲双胍通过调节胎球蛋白A、视黄醇结合蛋白4、脂滴包被蛋白和脂肪代谢相关基因,改善2型糖尿病引起的胰岛素抵抗。
引用
收藏
页码:1909 / 1914
页数:6
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