首页> 美国卫生研究院文献>Royal Society Open Science >Curcumin improves glycolipid metabolism through regulating peroxisome proliferator activated receptor γ signalling pathway in high-fat diet-induced obese mice and 3T3-L1 adipocytes
【2h】

Curcumin improves glycolipid metabolism through regulating peroxisome proliferator activated receptor γ signalling pathway in high-fat diet-induced obese mice and 3T3-L1 adipocytes

机译:姜黄素通过调节高脂饮食诱导的肥胖小鼠和3T3-L1脂肪细胞中的过氧化物酶体增殖物激活的受体γ信号传导途径改善糖脂代谢

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Curcumin is an active component derived from Curcuma longa L. which is a traditional Chinese medicine that is widely used for treating metabolic diseases through regulating different molecular pathways. Here, in this study, we aimed to comprehensively investigate the effects of curcumin on glycolipid metabolism in vivo and in vitro and then determine the underlying mechanism. Male C57BL/6 J obese mice and 3T3-L1 adipocytes were used for in vivo and in vitro study, respectively. Our results demonstrated that treatment with curcumin for eight weeks decreased body weight, fat mass and serum lipid profiles. Meanwhile, it lowered fasting blood glucose and increased the insulin sensitivity in high-fat diet-induced obese mice. In addition, curcumin stimulated lipolysis and improved glycolipid metabolism through upregulating the expressions of adipose triglyceride lipase and hormone-sensitive lipase, peroxisome proliferator activated receptor γ/α (PPARγ/α) and CCAAT/enhancer binding proteinα (C/EBPα) in adipose tissue of the mice. In differentiated 3T3-L1 cells, curcumin reduced glycerol release and increased glucose uptake via upregulating PPARγ and C/EBPα. We concluded that curcumin has the potential to improve glycolipid metabolism disorders caused by obesity through regulating PPARγ signalling pathway.
机译:姜黄素是源自姜黄的有效成分,姜黄是一种中药,通过调节不同的分子途径被广泛用于治疗代谢性疾病。在这里,在这项研究中,我们旨在全面研究姜黄素在体内和体外对糖脂代谢的影响,然后确定其潜在机制。雄性C57BL / 6BLJ肥胖小鼠和3T3-L1脂肪细胞分别用于体内和体外研究。我们的结果表明,用姜黄素治疗8周可降低体重,脂肪量和血清脂质谱。同时,它降低了高脂饮食诱导的肥胖小鼠的空腹血糖并提高了胰岛素敏感性。此外,姜黄素通过上调脂肪组织中甘油三酸酯脂肪酶和激素敏感性脂肪酶,过氧化物酶体增殖物激活受体γ/α(PPARγ/α)和CCAAT /增强子结合蛋白α(C /EBPα)的表达来刺激脂解并改善糖脂代谢。的老鼠。在分化的3T3-L1细胞中,姜黄素通过上调PPARγ和C /EBPα减少甘油的释放并增加葡萄糖的摄取。我们得出的结论是,姜黄素具有通过调节PPARγ信号通路改善肥胖引起的糖脂代谢紊乱的潜力。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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