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作 者:陈璐[1] 刘翠萍[1] 袁庆新[1] 徐宽枫[1] 刘超[1]
机构地区:[1]南京医科大学第一附属医院内分泌科,江苏南京210029
出 处:《南京医科大学学报(自然科学版)》2008年第3期278-281,共4页Journal of Nanjing Medical University(Natural Sciences)
基 金:江苏省医学重点学科资助项目(SK200214)
摘 要:目的:探讨母体营养不良对胎儿胰腺发育及功能的影响。方法:自妊娠11天起限制母鼠饮食(予正常50%)以建立宫内发育迟缓(intrauterine growth retardation,IUGR)新生大鼠模型。观察其生长发育状况,行葡萄糖耐量及胰岛素释放试验及免疫组化形态和量化分析,以评估IUGR新生大鼠胰腺发育情况及其功能变化。结果:IUGR组新生大鼠出生时体重、胰重和胰重/体重比值均明显低于正常组(P<0.001)。空腹血糖及胰岛素虽低于正常新生大鼠,但糖负荷后120min和180min血糖值下降慢于正常组[(18.95±2.63)mmol/Lvs(16.92±1.30)mmol/L,(18.29±2.58)mmol/Lvs(15.87±2.08)mmol/L,P均<0.05]。同时,IUGR组胰腺组织中胰岛素阳性表达细胞面积[(M=1530.98μm2,QU-L=2961.98μm2)vs(M=3146.24μm2,QU-L=4633.73μm2)]及胰岛素染色阳性率[(M=2.03%,QU-L=2.67%)vs(M=5.44%,QU-L=4.34%)]亦小于正常组(P均<0.01)。结论:母体营养不良导致IUGR新生大鼠胰腺发育受损,胰岛面积减少,血糖调节能力下降。Objective:To study the effects of maternal malnutrition on the development and function of fetal pancreas. Methods: The newborn rat model with intrauterine growth retardation was established by maternal nutrition restriction(50% calorie restriction of the normal) during the 11^th to 21^st days of pregnancy. The growth and development status of the newborns,glucose tolerance test and immunohistochemistry analysis were investigated to evaluate the development and function of fetal pancreas. Results:Body,pancreas weight and the ratio of pancreas to body weight of newborns in IUGR group were much lower than those in normal group(P 〈 0,001 ). The fasting glucose and insulin levels of IUGR newborns were both lower than those of normal ones,whereas glucose levels at 120 min and 180 min after glucose challenge were significantly higher in IUGR group [(18.95 ±2.63)mmol/L vs (16.92 ± 1.30)mmol/L; (18.29 ± 2.58)mmol/L vs (15.87± 2.08)mmol/L,P 〈 0.05]. In addition,areas of insulin-expression positive cells[(M=l 530.98μm^2, Qu-L=2 961.98 μm^2)vs (M=3 146.24 μm^2,QU-L=4 633.73 μm^2) l and positive rate of cells staining with insulin [(M=2,03%,QU-L= 2.67%)vs(M=5.44%, QU-L=4.34%)] were also less than normal newborns(P 〈 0.01 ). Conclusion:Maternal malnutrition would lead to impaired pancreatic development and decreased islet area in newborn rats, as well as dysfunction of glucose regulatory capacity.
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