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作 者:刘勇[1] 马丹丹[1] 梅洪亮[1] 张建新[1] 蔡逊[1] 邵俊伟[1]
机构地区:[1]广州军区武汉总医院普通外科,湖北武汉430070
出 处:《华南国防医学杂志》2016年第6期359-361,共3页Military Medical Journal of South China
基 金:湖北省自然科学基金项目(2010CDB09201)
摘 要:目的观察回肠转位术(ileal transposition,IT)对非肥胖型2型糖尿病GK大鼠的血糖及胰高血糖素样肽-1(glucagon-like peptide-1,GLP-1)的影响,探讨IT对GK大鼠的降糖作用及其可能的机制。方法随机数字表法将20只雄性正常体质量GK大鼠分为回肠转位术组(IT组)和假手术组(Sham组),每组10只。观察并测定两组GK大鼠术前及术后1周、2周、1个月、2个月、3个月、6个月的体质量、空腹血糖(fasting blood glucose,FBG)、血清胰岛素(fasting insulin,INS)、糖化血红蛋白(glycosylated hemoglobin,HbA1c)、GLP-1水平的变化。结果 IT组与Sham组手术前后体质量比较无统计学差异(P>0.05)。与术前比较,术后1周~6个月IT组GK大鼠FBG明显降低(P<0.05),空腹GLP-1明显升高(P<0.05),术后3个月和6个月HbA1c明显降低(P<0.05)、INS水平明显升高(P<0.05)。Sham组上述指标均未见明显变化。结论 IT对GK大鼠有明显的降糖作用,其机制可能是食物提前进入回肠,刺激GLP-1分泌增加,从而促进胰岛素释放,促进β细胞增生并抑制其凋亡。Objective To observe the effect of ileal transposition(IT) surgery on blood glucose and glucagon-like peptide-1 (GLP-1) expression in Goto-Kakizaki (GK) rats with non-obese type 2 diabetes mellitus (T2DM), and investigate the hypoglycemic effect and possible mechanisms. Methods Male GK rats were randomly divided into IT surgery group (n= 10) and Sham operation group (n = 10). The body weight , fasting blood glueose(FBG), fasting insulin (INS), glycosylated hemoglobin( HbAl c) levels and glucagon-like peptide-1 (GLP-1) levels of the two groups GK rats were determined before operation and at 1 week, 2 weeks, 1 month, 2 months, 3 months, 6 months after operations. Results There was no significant difference in the body weight in IT surgery group(P〉0. 05). FBG levels were significantly decreased in 1-24 weeks after the operation in IT surgery group(P〈0. 05). GLP-1 expression was significantly increased after the operation(P〈0. 05). HbAlc level was decreased in 3 months and 6 months after the operation(P〈 0. 05). The INS levels were increased in 3 months and 6 months after the operation(P^0. 05). The all parameters of sham operation group did not change. Conclusion IT surgery on GK rates has a significant hypoglyeemic effect. IT surgery makes the food fast pass to the ileum and stimulates the GLP-1 secretion. The increase of GLP-1 may help to in- crease insulin, induce the apoptosis and inhibit the proliferation of beta cells.
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