维生素D缺乏导致小鼠糖代谢异常

Vitamin D deficiency induces the impairment of glucose metabolism in mouse

目的研究1α羟化酶基因敲除小鼠的糖代谢,分析维生素D在糖代谢中的作用。方法采用1α羟化酶基因敲除小鼠,禁食过夜后,按2g/kg剂量的葡萄糖灌胃。灌胃后0、15、30、60、120min尾部取血,测定血糖。灌胃后0、15、60min眼球取血,分离血清,放免法测定胰岛素水平。不禁食的小鼠腹腔注射0.75U/kg剂量的胰岛素。注射后0、15、30、60min取尾血、测定血糖。分析不同基因型小鼠对外原性胰岛素的敏感性。常规石蜡切片观察小鼠胰岛淋巴细胞浸润情况。结果基因敲除小鼠基础糖代谢与野生型小鼠无明显差异。但在糖负荷后,胰岛素分泌相对不足,血糖水平显著升高。两种小鼠的胰岛素敏感性无明显差别。基因敲除小鼠胰岛未发现淋巴细胞浸润。结论维生素D缺乏损害了小鼠的糖代谢。

Objective To investigate the role of vitamin D on the physiology of glucose metabolism in mouse. Methods 1 alpha hydroxylase gene knockout mice （KO group）aged 8 weeks versus wild type （WT）mice were used in,this study. Oral glucose tolerance was analyzed after intragastrically giving 2g glucose/kg body wt in fasting state. Blood glucose and insulin were measured at 0, 15, 30, 60, and 120 min after glucose administration. Irttraperitoneal injection of insulin of 0. 75 units/kg was performed on 8- week-old mice in the non-fasting state. Blood glucose was measured at 0, 15, 30, and 60 rain after insulin administration. The paraffin-infiltrated pancreas were sectioned and stained by hematoxylin eosin. Results In glucose tolerance tests, baseline blood glucose levels were unchanged in fasting KO versus WT mice. However, after oral glucose loading, blood glucose level in KO mice was higher and maximum serum insulin levels were lower significantly than wild type mice. Sensitivity to exogenous insulin was similar in both groups. Lymphocyte infiltration in pancreatic islets was not found in both groups. Conclusion Vitamin D deficiency can result in impaired glucose metabolism.