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作 者:孙进[1] 李凤飞[1] 朱红红[1] 李建民[2] 马建华[1]
机构地区:[1]南京医科大学附属南京医院内分泌科,江苏南京210006 [2]南京医科大学江苏省医药动物实验基地,江苏南京211166
出 处:《南京医科大学学报(自然科学版)》2016年第4期416-419,共4页Journal of Nanjing Medical University(Natural Sciences)
基 金:中国博士后科学基金资助(2015M581829)
摘 要:目的 :建立胰岛β细胞特异性失活PPACα基因小鼠模型,对其表型进行初步观察。方法 :通过Ins2-Cre小鼠与PP2ACα^(^(flox/flox))小鼠交配,获得胰岛β细胞特异性失活PP2ACα基因小鼠(PP2ACα^(flox/fIox):Ins2-Cre)。PCR和Western blot鉴定PP2ACα基因第二外显子敲除小鼠(KO)。4月龄时行腹腔注射葡萄糖耐量试验(IPGTT),以PP2ACα^(flox/flox)小鼠为对照。结果 :1PP2ACα转录本在KO小鼠短于对照小鼠;2KO小鼠胰岛中PP2AC蛋白水平较对照小鼠显著下降(P<0.05);3IPGTT结果显示:4月龄KO小鼠30、60、120 min时血糖明显高于对照小鼠(P<0.05)。结论:成功建立胰岛β细胞特异性失活PPACα基因小鼠模型,4月龄PP2ACα^(flox/fIox):Ins2-Cre小鼠糖耐量受损。Objective:To establish mouse model of PP2AC gene specifical inactivation in pancreatic cells and investigate preliminary animal phenotype. Methods: The Ins-2 transgenic mice in which Cre enzyme was exclusively detected in pancreatic-cells bred with PP2ACα^flox/flox mice to obtain PP2ACα^lox/+:Ins-2 mice, then bred with the PP2ACα^flox/flox mice again to obtain PP2ACα^flox/flox:Ins-2 mice(KO mice). We identified the 2nd exon of PP2ACα knockdown by PCR and Western Blot. Interperitoneal glucose tolerance test(IPGTT) was performed in transgenic mice at 4 months, and PP2ACα^flox/flox mice were employed with control. Results: PP2ACα transcripts were shorter in KO mice than those in control mice. The protein level of PP2AC expression in KO mice was significantly lower than that of control mice(P〈0.05). The results of IPGTT indicated that the blood glucose levels at 30 min, 60 min and 120 min were significantly higher than those of controls(P〈0.05). Conclusion: Specifical inactivation of PP2AC in pancreatic β-cells mouse model is successfully established, and glucose tolerance impairs at 4 months in PP2ACα^flox/flox:Ins2-Cre mice.
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