...
首页> 外文期刊>The Journal of Nutritional Biochemistry >A high-fish-oil diet prevents adiposity and modulates white adipose tissue inflammation pathways in mice
【24h】

A high-fish-oil diet prevents adiposity and modulates white adipose tissue inflammation pathways in mice

机译:高鱼油饮食可防止肥胖并调节小鼠的白色脂肪组织炎症途径

获取原文
获取原文并翻译 | 示例
           

摘要

Fish oil improves obesity and its comorbidities, but its mechanisms of action remain unknown. We evaluate the effects of a diet rich in fish oil in white adipose tissue (WAT) inflammation pathways, renin-angiotensin system (RAS) and mitogen-activated protein kinases (MAPKs). To achieve our aims, four groups of male C57BL/6 mice were fed different diets: standard chow diet (SC; 10% energy from fat), SC+fish oil diet (SC-FO; 10% energy from fat), high-fat lard diet (HF-L; 50% energy from lard) and HF fish oil diet (HF-FO; 50% energy from fish oil). We evaluated body mass, epididymal fat pad mass, food intake and glucose tolerance. In WAT, we assessed adipocyte hypertrophy, monocyte chemotactic protein-1 immunofluorescence, and gene and protein expression of insulin signaling, inflammation, MAPKs, RAS, peroxisome proliferator-activated receptors (PPARs) and AMP-activated protein kinase (AMPK). In relation to the results, the HF-L group, as expected, showed elevated body mass and adiposity, glucose intolerance and hypertrophied adipocytes. In WAT, we found a defect in insulin signaling, infiltration of macrophages and inflammatory markers with the associated activation of MAPKs and local RAS. On the contrary, the HF-FO group did not present increased body mass, adiposity or glucose intolerance. In this group, insulin signaling, macrophage infiltration and inflammation were reduced in WAT in comparison with the HF-L group. We also observed decreases of MAPKs and local RAS and elevation of PPAR and AMPK. In summary, fish oil activates PPAR (the three isoforms) and AMPK, decreases WAT insulin resistance and inflammation, and inhibits MAPK and RAS pathways activation. (C) 2015 Elsevier Inc. All rights reserved.
机译:鱼油可改善肥胖症及其合并症,但其作用机理仍然未知。我们评估了在白色脂肪组织(WAT)炎症途径,肾素-血管紧张素系统(RAS)和促分裂原激活蛋白激酶(MAPKs)中富含鱼油的饮食的影响。为了实现我们的目标,给四组雄性C57BL / 6小鼠喂了不同的饮食:标准的日常饮食(SC; 10%的脂肪能量),SC +鱼油的饮食(SC-FO; 10%的脂肪能量),高脂饮食。脂肪猪油饮食(HF-L;猪油能量为50%)和HF鱼油饮食(HF-FO;鱼油能量为50%)。我们评估了体重,附睾脂肪垫质量,食物摄入量和葡萄糖耐量。在WAT中,我们评估了脂肪细胞肥大,单核细胞趋化蛋白1免疫荧光以及胰岛素信号,炎症,MAPK,RAS,过氧化物酶体增殖物激活受体(PPAR)和AMP激活蛋白激酶(AMPK)的基因和蛋白表达。与结果相关,HF-L组如预期的那样显示出体重和脂肪增加,葡萄糖耐量下降和肥大的脂肪细胞。在WAT中,我们发现了胰岛素信号传导,巨噬细胞浸润和炎性标志物的缺陷以及相关的MAPK和局部RAS激活。相反,HF-FO组未出现体重增加,肥胖或葡萄糖耐量增加。与HF-L组相比,WAT组胰岛素信号,巨噬细胞浸润和炎症减少。我们还观察到MAPKs和局部RAS的降低以及PPAR和AMPK的升高。总之,鱼油可激活PPAR(三种同工型)和AMPK,降低WAT胰岛素抵抗和炎症,并抑制MAPK和RAS途径的激活。 (C)2015 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