...
首页> 外文期刊>Life sciences >Effect of maternal obesity on diabetes development in adult rat offspring
【24h】

Effect of maternal obesity on diabetes development in adult rat offspring

机译:母体肥胖对成年大鼠后代糖尿病发展的影响

获取原文
获取原文并翻译 | 示例

摘要

This study aimed to evaluate whether maternal obesity leads to the onset of diabetes in adult Wistar rats offspring. MSG solution neonatally administration induced obesity in rats (F(1)MSG group, n = 30); and saline solution was also administrated to control rats (F1CON group, n = 13). In 3rd month of age, both control and MS G groups were mated for offspring (generation FA named as F2CON, n = 28 and F(2)MSG groups, n = 15; and so both generations were studied until 7th month of life. Lee Index was measured for experimental obesity validation from 5th to 7th month. Glycemia was weekly determined during pregnancy and monthly from 3rd to 7th month. In the end of experimental period all rats were submitted to oral glucose tolerance test (OGTT), with estimation of total area under the curve (AUC); and insulin tolerance test (ITT). Rats were then anesthetized and killed. Data were statistically analyzed with significance level of p < 0.05. Lee Index has confirmed obesity in all MSG rats. Glycemic levels comparisons between generations showed significant maternal interference in control and MSG groups. OGTT analysis showed higher glycemia in obese rats (F(1)MSG) and their offspring (F(2)MSG) as compared to their respective controls; and MSG groups increased AUC from OGTT. As regards ITT, F(2)MSG showed higher glycemia at 30 and 120 min, suggesting a delay of insulin action decreasing. Although glucose intolerance and insulin resistance clinical conditions represent as a factors for type 2 Diabetes mellitus development, this experimental model proposal was not efficient to induce type 2 Diabetes mellitus, but for obesity developing, glucose intolerance and insulin resistance in successive generations of rats. (c) 2007 Elsevier Inc. All rights reserved.
机译:这项研究旨在评估母体肥胖是否会导致成年Wistar大鼠后代患上糖尿病。 MSG溶液新生儿给药诱发大鼠肥胖(F(1)MSG组,n = 30);对照组也给予盐溶液(F1CON组,n = 13)。在第3个月大时,对照组和MS G组都为后代交配(FA代名为F2CON,n = 28,F(2)MSG组,n = 15;因此对这两个代进行了研究,直到生命的第7个月。在第5个月至第7个月测量Lee指数以进行实验性肥胖验证;在怀孕期间每周测定一次血糖;在第3个月至第7个月每月测定一次血糖。曲线下的总面积(AUC);胰岛素耐受性试验(ITT),然后将其麻醉并处死,统计学分析数据的显着性水平为p <0.05。Lee指数已证实所有MSG大鼠均肥胖,血糖水平之间的比较几代人在对照组和味精组中显示出明显的母体干扰; OGTT分析显示,肥胖大鼠(F(1)MSG)及其后代(F(2)MSG)的血糖水平高于其相应对照组; MSG组增加了OGTT的AUC 。关于ITT,F(2)MSG在30和120分钟时显示出较高的血糖,表明胰岛素作用延迟延迟。尽管葡萄糖耐量和胰岛素抵抗的临床状况是2型糖尿病发展的一个因素,但该实验模型建议并不能有效地诱导2型糖尿病,但对于肥胖的发展,连续几代大鼠的糖耐量和胰岛素抵抗。 (c)2007 Elsevier Inc.保留所有权利。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号