• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Journal of Nutritional Biochemistry >Maternal high-fat feeding through pregnancy and lactation predisposes mouse offspring to molecular insulin resistance and fatty liver.
【24h】

Maternal high-fat feeding through pregnancy and lactation predisposes mouse offspring to molecular insulin resistance and fatty liver.

机译：孕期和哺乳期的孕妇高脂喂养使小鼠后代容易患分子胰岛素抵抗和脂肪肝。

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

The exposure to an increased supply of nutrients before birth may contribute to offspring obesity. Offspring from obese dams that chronically consume a high-fat diet present clinical features of metabolic syndrome, liver lipid accumulation and activation of c-Jun N-terminal kinases (JNK) consistent with the development of nonalcoholic fatty liver disease (NAFLD). However, in spite of the importance of the resistance to insulin for the development of NAFLD, the molecular alterations in the liver of adult offspring of obese dams are yet to be investigated. In this study, we tested the hypothesis that the consumption of excessive saturated fats during pregnancy and lactation contributes to adult hepatic metabolic dysfunction in offspring. Adult male offspring of dams fed a high-fat diet (HN) during pregnancy and lactation exhibited increased fat depot weight; increased serum insulin, tumor necrosis factor alpha and interleukin 1 beta; and reduced serum triglycerides. Liver showed increased JNK and I kappa B kinase phosphorylation and PEPCK expression in the adult. In addition, liver triglyceride content in the offspring 1 week after weaning and in the adult was increased. Moreover, basal ACC phosphorylation and insulin signaling were reduced in the liver from the HN group as compared to offspring of dams fed a standard laboratory chow (NN). Hormone-sensitive lipase phosphorylation (Ser565) was reduced in epididymal adipose tissue from the HN group as compared to the NN group. It is interesting that all changes observed were independent of postweaning diet in 14-week-old offspring. Therefore, these data further reinforce the importance of maternal nutrition to adult offspring health.
机译：出生前接触营养增加的供应可能会导致后代肥胖。长期食用高脂饮食的肥胖大坝的后代表现出代谢综合征，肝脂质蓄积和c-Jun N端激酶（JNK）活化的临床特征，这与非酒精性脂肪肝疾病（NAFLD）的发展一致。然而，尽管胰岛素抵抗对NAFLD的发展很重要，但肥胖大坝成年后代肝脏中的分子变化尚待研究。在这项研究中，我们检验了以下假设：怀孕和哺乳期间摄入过多的饱和脂肪会导致后代的成人肝代谢功能障碍。在怀孕和哺乳期间饲喂高脂饮食（HN）的水坝成年雄性后代表现出增加的脂肪库体重;血清胰岛素，肿瘤坏死因子α和白介素1β升高;并降低血清甘油三酸酯。成年人肝脏中JNK和IκB激酶的磷酸化和PEPCK表达增加。另外，断奶后1周和成年后代的肝脏甘油三酸酯含量增加。此外，与喂食标准实验室食物（NN）的母鼠的后代相比，HN组肝脏的基础ACC磷酸化和胰岛素信号转导减少。与NN组相比，HN组附睾脂肪组织中的激素敏感性脂肪酶磷酸化（Ser565）减少。有趣的是，观察到的所有变化均与14周龄后代的断奶后饮食无关。因此，这些数据进一步加强了母亲营养对成年后代健康的重要性。

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