• 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 >Luteolin reduces adipose tissue macrophage inflammation and insulin resistance in postmenopausal obese mice
【24h】

Luteolin reduces adipose tissue macrophage inflammation and insulin resistance in postmenopausal obese mice

机译：叶黄素在绝经后肥胖小鼠中减少了脂肪组织巨噬细胞炎症和胰岛素抗性

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

Previously, we showed that loss of ovarian function in mice fed high-fat diet exacerbated insulin resistance and adipose tissue inflammation. In the current study, we tested whether consumption of luteolin, an anti-inflammatory flavonoid, could mitigate adipose tissue inflammation and insulin resistance in obese ovariectomized mice. Nine-week-old ovariectomized C57BL/6 mice were fed a low-fat diet, high-fat diet (HFD) or HFD supplemented with 0.005% luteolin (HFD +L) for 16 weeks. Results showed no difference in body weight or fat mass between mice fed HFD+L and those fed HFD. However, luteolin supplementation resulted in lower CD11c(+) macrophages in gonadal adipose tissue, as well as a trend toward lower macrophage infiltration. Luteolin supplementation also significantly lowered mRNA expression of inflammatory and M1 markers MCP-1, CD11c, TNF-alpha and IL-6, while maintaining expression of M2 marker MGL1. Consistent with this, the in vitro luteolin treatment, with or without the presence of estrogen, inhibited lipopolysaccharide-induced polarization of RAW 264.7 cells toward M1 phenotype. We further found that luteolin supplementation protected mice from insulin resistance induced by HFD consumption; this improved insulin resistance was correlated with reductions in CD11c(+) adipose tissue macrophages. Taken together, these findings indicate that dietary luteolin supplementation attenuates adipose tissue inflammation and insulin resistance found in mice with loss of ovarian function coupled with an HFD intake, and this effect may be partly mediated through suppressing M1-like polarization of macrophages in adipose tissue. These results have clinical implication in implementing dietary intervention for prevention of metabolic syndrome associated with postmenopause and obesity. (C) 2019 Elsevier Inc. All rights reserved.
机译：以前，我们表明，喂养高脂饮食的小鼠中卵巢功能的丧失加剧了胰岛素抵抗和脂肪组织炎症。在目前的研究中，我们测试了虎蛋白的消费，抗炎黄酮类化合物是否可以减轻肥胖的卵巢切除小鼠的脂肪组织炎症和胰岛素抗性。将九周卵巢切除的C57BL / 6小鼠喂养低脂饮食，高脂饮食（HFD）或HFD，其补充有0.005％的叶英蛋白（HFD + L）16周。结果表明，喂养HFD + L和喂养HFD的小鼠之间的体重或脂肪质量没有差异。然而，叶黄素补充导致Gonadal脂肪组织中的降低CD11c（+）巨噬细胞，以及较低巨噬细胞浸润的趋势。叶黄素补充还显着降低炎症和M1标记MCP-1，CD11C，TNF-α和IL-6的mRNA表达，同时保持M2标记MGL1的表达。与此一致，具有或不存在雌激素的体外曲霉治疗，抑制脂多糖诱导的原料264.7细胞的偏振朝向M1表型。我们进一步发现，从HFD消费诱导的胰岛素抵抗诱导的小鼠受到胰岛素的补充;这种改善的胰岛素抵抗与CD11C（+）脂肪组织巨噬细胞的降低相关。这些发现表明，膳食叶黄素补充剂衰减脂肪组织炎症和小鼠中发现的卵巢功能丧失与HFD摄入量的损失，并且这种效果可以通过抑制脂肪组织中的巨噬细胞的M1样极化部分介导。这些结果具有临床意义，实施饮食干预以预防与后期和肥胖相关的代谢综合征。 （c）2019 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