• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Dietary fructose accelerates the development of diabetes in UCD-T2DM rats: Amelioration by the antioxidant, α-lipoic acid
【24h】

Dietary fructose accelerates the development of diabetes in UCD-T2DM rats: Amelioration by the antioxidant, α-lipoic acid

机译：饮食中的果糖可促进UCD-T2DM大鼠的糖尿病发展：抗氧化剂α-硫辛酸的改善

获取原文
获取原文并翻译 | 示例
       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Sustained fructose consumption has been shown to induce insulin resistance and glucose intolerance, in part, by promoting oxidative stress. Alpha-lipoic acid (LA) is an antioxidant with insulin-sensitizing activity. The effect of sustained fructose consumption (20% of energy) on the development of T2DM and the effects of daily LA supplementation in fructose-fed University of California, Davis-Type 2 diabetes mellitus (UCDT2DM) rats, a model of polygenic obese T2DM, was investigated. At 2 mo of age, animals were divided into three groups: control, fructose, and fructose + LA (80 mg LA?kg body wt -1·day-1). One subset was followed until diabetes onset, while another subset was euthanized at 4 mo of age for tissue collection. Monthly fasted blood samples were collected, and an intravenous glucose tolerance test (IVGTT) was performed. Fructose feeding accelerated diabetes onset by 2.6 ± 0.5 mo compared with control (P 0.01), without affecting body weight. LA supplementation delayed diabetes onset in fructosefed animals by 1.0 ± 0.7 mo (P 0.05). Fructose consumption lowered the GSH/GSSG ratio, while LA attenuated the fructoseinduced decrease of oxidative capacity. Insulin sensitivity, as assessed by IVGTT, decreased in both fructose-fed and fructose + LA-supplemented rats. However, glucose excursions in fructose-fed LA-supplemented animals were normalized to those of control via increased glucose-stimulated insulin secretion. Fasting plasma triglycerides were twofold higher in fructose-fed compared with control animals at 4 mo, and triglyceride exposure during IVGTT was increased in both the fructose and fructose + LA groups compared with control. In conclusion, dietary fructose accelerates the onset of T2DM in UCD-T2DM rats, and LA ameliorates the effects of fructose by improving glucose homeostasis, possibly by preserving β-cell function.
机译：事实证明，持续摄入果糖会部分地通过促进氧化应激而引起胰岛素抵抗和葡萄糖耐受不良。 α-硫辛酸（LA）是具有胰岛素敏感性的抗氧化剂。持续摄入果糖（能量的20％）对T2DM发育的影响以及每日补充果糖的加州大学戴维斯2型糖尿病（UCDT2DM）大鼠（多基因肥胖T2DM模型）的影响，被调查了。在2月龄时，将动物分为三组：对照组，果糖和果糖+ LA（80 mg LA？kg体重-1·day-1）。跟踪一个亚组直至糖尿病发作，而另一亚组在4 mo岁时被安乐死以收集组织。每月收集空腹血样，并进行静脉葡萄糖耐量测试（IVGTT）。与对照组相比，果糖喂养使糖尿病发作加快了2.6±0.5 mo（P <0.01），而没有影响体重。 LA补充剂使果蝇动物的糖尿病发作延迟1.0±0.7 mo（P <0.05）。果糖消耗降低了GSH / GSSG比，而LA减弱了果糖引起的氧化能力下降。通过IVGTT评估，果糖喂养和果糖+ LA补充大鼠的胰岛素敏感性均下降。然而，通过增加葡萄糖刺激的胰岛素分泌，将果糖喂养的补充了LA的动物中的葡萄糖偏移归一化为对照。 4个月时，果糖喂养的空腹血浆甘油三酯比对照组动物高两倍，果糖和果糖+ LA组的IVGTT期间甘油三酸酯暴露均高于对照组。总之，饮食中的果糖可促进UCD-T2DM大鼠T2DM的发作，而LA可通过改善葡萄糖体内稳态（可能通过保持β细胞功能）来改善果糖的作用。

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