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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 a murine model of pancreatic islet β cell-specific inactivation of PPACα gene and preliminary observation of its phenotype. Methods: Pancreatic β-cell-specific inactivated PP2ACα mice (PP2ACα ~ (flox / fox): Ins2-Cre) were obtained by mating the Ins2-Cre mice with PP2ACα ~ (flox / flox) mice. PCR and Western blot were used to identify PP2ACα gene exon 2 knockout mice (KO). At 4 months of age, intraperitoneal glucose tolerance test (IPGTT) was performed, and PP2ACα ~ (flox / flox) mice were used as controls. Results: 1PP2ACα transcripts were shorter in KO mice than in control mice; PP2AC protein levels in 2KO mice was significantly decreased compared with control mice (P <0.05); 3IPGTT results showed that: 4 months old KO mice 30,60,120 Blood glucose was significantly higher than the control mice (P <0.05). CONCLUSION: PPARα gene mouse model of islet β cell-specific inactivation was successfully established, and impaired glucose tolerance of 4-month-old flox / fox: Ins2-Cre mice.