摘要
目的:了解母鼠孕期营养不良所致宫内生长迟缓(intrauterinegrowthretardation,IUGR)大鼠成年后胰岛β细胞分泌功能及胰岛素敏感性变化。方法:采用妊娠第1天Wistar孕鼠以对照组孕鼠50%的饲料喂养建立IUGR模型,以低于对照组新生鼠出生体重均值的2个标准差判断为IUGR。以子代12～15周成年雄鼠为实验对象,采有葡萄糖耐量试验和正常血糖高胰岛素钳夹技术,计算胰岛β细胞功能数(ModifiedBeta-CellfunctionIndex,MBCI)、胰岛素介导的稳态葡萄糖输注率(steady-stateglucoseinfusionrate,SSGIR,mg/(kg·min),对胰岛β细胞分泌功能及外周组织胰岛素敏感性进行评价。结果:(1)饥饿组新生鼠平均出生体重明显低于对照组均值的2SD(4.37±0.34gvs6.42±0.2g,P<0.001),为IUGR。至12～15周时IUGR组体重仍低于对照组(279.8±30.3vs341.3±36.6g,P<0.01);到成年期约有25%IUGR幼鼠死亡;(2)饥饿组幼鼠成年后(12～15周)胰岛β细胞功能指数与对照组比较差别无显著性(66.52±21.66vs57.43±10.82,P=0.286);饥饿组幼鼠成年期SSGIR明显低于对照组(9.97±2.65mg/(kg·min)vs22.55±4.05mg/(kg·min),P<0.001)。结论:母鼠孕期营养不良导致胎鼠宫内生长迟缓并延续至成年期;
Objective:To investigate the endocrine functions of the islet β cells and insulin sensitivity in the adult male rats,with intrauterine growth retardation induced by maternal starvation during pregnancy.Methods:The foods were available ad libitum throughout the pregnancy to the control group(n=8) and the rats in the experimental group(n=9) were fed 50% of the control group.The average birth weight of the offspring in the experimental group were below the mean values of the birth weights of the control group more than 2SD,defined as IUGR.The glucose tolerance test and hyperinsulinemic-euglycemic clamp were done in the adult male offspring(n=9 for each group).Results:(1)Litter size was not affected by maternal undernutrition.The birth weights of the rats in the maternal starvation during the pregnancy were significantly lower(4.37±0.34g)than those in the control group(6.42±0.29g) as defined as IUGR.The postnatal survival rate of the IUGR rats(75.4%) is significantly lower than that of the normal offspring(94.9%).The mean weight of the IUGR male rats was still lower than that of control group (279.8±30.3g vs 341.3±36.6g,P<0.01) until week 12 postnatally;(2)There were no significant differences in the values of MBCI between the two groups(66.52±21.66 vs 57.43±10.82,P=0.286).The values of SSGIR in the IUGR rats were lower than that in the normal rats(9.97±2.65 mg/(kg·min) vs 22.55±4.05 mg/(kg·min),P<0.001).Conclusion:Maternal malnutrition during pregnancy caused intrauterine growth retardation in the fetus.The male rats with IUGR did not achieve catch up growth even in the adult life.Though there was no significant difference in the β cell endocrine function,the IUGR rats developed severer insulin resistance in their adult life which is closely related to the metabolic syndrome.
出处
《重庆医科大学学报》
CAS
CSCD
2005年第3期359-362,共4页
Journal of Chongqing Medical University
基金
重庆医科大学优秀博士论文科研基金资助
关键词
宫内生长迟缓
胰岛素抵抗
疾病模型
动物
Intrauterine growth retardation
Insulin resistance
Disease model
Animal
