不同血糖状态下的妊娠小鼠脂代谢特点与肝脏病理学特征

目的通过高脂高糖诱导妊娠糖尿病（GDM）小鼠模型,探讨不同血糖状态下的妊娠小鼠脂代谢特点及其肝脏的病理学特征。方法将C57BL/6J雌鼠随机分为普通饮食组和高脂高糖饮食组,确定受孕后,普通饮食组继续给予普通饲料喂养,高脂高糖饮食组给予高脂高糖饲料喂养。检测孕期体重情况、空腹血糖、空腹胰岛素,计算胰岛素抵抗指数,同时检测甘油三酯、胆固醇和游离脂肪酸,并且进行肝脏组织病理学观察。结果高脂高糖饮食喂养孕鼠组空腹血糖水平明显升高且高血糖水平较稳定,体重增加明显,妊娠晚期胰岛素水平及胰岛素抵抗指数增加,动物模型稳定。高脂高糖饮食孕鼠组小鼠血甘油三酯、总胆固醇和游离脂肪酸较高脂高糖饮食未孕组小鼠、普通饮食未孕组小鼠及普通饮食孕鼠组小鼠明显增高。肝脏组织病理显示,高脂高糖饮食孕鼠组肝板排列不整齐,肝细胞胞浆内可见大小不等的脂肪空泡。结论运用高脂高糖饮食诱导C57BL/6J小鼠能够模拟人类GDM发病特点在不同饲养方式和不同学堂状态下的妊娠小鼠脂质代谢紊乱不一致,GDM小鼠其血脂代谢紊乱程度严重,并且可以引起明显的肝脏病理学变化。

The lipid metabolism characteristic and liver pathological feature of pregnant mouse under the condition of different blood glucose level

Objective To establish a gestational diabetes mouse model by feeding high fat and high sugar diet,and to explore the lipid metabolism characteristic and liver pathological feature of different blood glucose in mouse. Methods C57BL/6J female mice were randomly divided into normal diet group and high fat and high sugar feeding group ： after successful pregnancy, the normal diet group were offered a normal feed, and high fat and sugar diet group were fed with high fat and sugar. The body weight, fasting plasma glucose and fasting insulin were measured, and the insulin resistance index was calculated. At the same time, the triglycerides, cholesterol and free fatty acids were detected, and the pathological liver tissues were observed. Results High fat and high sugar diet for pregnant mice were significantly higher in fasting glucose levels and its hyperglycemia levels were more stable. The body weight increased significantly, and the insulin level and insulin resistance index increased during third trimester of pregnancy, and the animal model was stable. The measure of blood triglycerides,total cholesterol and free fatty acids showed significant increase in high fat and high sugar diet group of pregnant mice compared with high fat and high sugar diet non - pregnant group, normal diet non - pregnant group and normal diet pregnant group. Liver histopathology showed that hepatic plate arranged irregularly and ranging from the size of the fat vacuole within cytoplasm of liver cells. Conclusion The induced C57BL/6J mice by application of high fat and high sugar diet can simulate the characteristics of human GDM disease. The lipid metabolism disorder is not consistent in different feeding way and the different blood glucose condition of pregnant mice. The disorder of lipid metabolism is very serious in GDM mice, and can cause significant changes in liver pathology.