Dietary carnosic acid suppresses hepatic steatosis formation via regulation of hepatic fatty acid metabolism in high-fat diet-fed mice.
Dietary carnosic acid suppresses hepatic steatosis formation via regulation of hepatic fatty acid metabolism in high-fat diet-fed mice.
复制标题
DOI：
10.4162/nrp.2013.7.4.294
复制
发表时间：
2013-08
影响因子：
2.4
通讯作者：
Mun ST
中科院分区：
文献类型：
--
作者：
Park MY;Mun ST
在这项研究中，我们研究了鼠尾草酸（CA），迷迭香（迷迭香）叶的酚类化合物，肝脏抗脂肪变性活性，以及其可能的作用机制，在高脂饮食（HFD）喂养的小鼠模型。给小鼠喂食HFD或补充有0.01%（w/w）CA或0.02%（w/w）CA的HFD，持续12周，之后评价体重、血脂谱和脂肪酸机制标志物的变化。0.02%（w/w）CA饮食导致脂肪变性等级以及胰岛素抵抗（HOMA-IR）指数值、腹膜内葡萄糖耐量试验（IGTT）结果、体重增加、肝脏重量和血脂水平的稳态模型评估显著下降（P < 0.05）。肝脂肪生成基因如固醇调节元件结合蛋白-1c的表达水平0.01%（w/w）CA和0.02%（w/w）CA饲料组的SREBP-1c、肝脏脂肪酸结合蛋白（L-FABP）、硬脂酰辅酶A去饱和酶1（SCD 1）和脂肪酸合成酶（FAS）显著低于HFD组;另一方面，与HFD组相比，饲喂0.02%（w/w）CA饲料的小鼠，过氧化物酶体增殖物激活受体α（PPAR-α）、肉毒碱棕榈酰转移酶1（CPT-1）和酰基辅酶A氧化酶（ACO）等β-氧化相关基因的表达水平升高（P < 0.05）。此外，与HFD组相比，饲喂0.02%（w/w）CA饲料的小鼠肝脏中棕榈酸（C16：0）、棕榈油酸（C16：1）和油酸（C18：1）的含量显著降低（P < 0.05）。这些结果表明，口服给予CA通过减少小鼠体内从头脂肪生成和脂肪酸延长以及增加脂肪酸β-氧化来抑制HFD诱导的肝脂肪变性和脂肪肝相关代谢紊乱。
In this study, we examined the hepatic anti-steatosis activity of carnosic acid (CA), a phenolic compound of rosemary (Rosmarinus officinalis) leaves, as well as its possible mechanism of action, in a high-fat diet (HFD)-fed mice model. Mice were fed a HFD, or a HFD supplemented with 0.01% (w/w) CA or 0.02% (w/w) CA, for a period of 12 weeks, after which changes in body weight, blood lipid profiles, and fatty acid mechanism markers were evaluated. The 0.02% (w/w) CA diet resulted in a marked decline in steatosis grade, as well as in homeostasis model assessment of insulin resistance (HOMA-IR) index values, intraperitoneal glucose tolerance test (IGTT) results, body weight gain, liver weight, and blood lipid levels (P < 0.05). The expression level of hepatic lipogenic genes, such as sterol regulating element binding protein-1c (SREBP-1c), liver-fatty acid binding protein (L-FABP), stearoyl-CoA desaturase 1 (SCD1), and fatty acid synthase (FAS), was significantly lower in mice fed 0.01% (w/w) CA and 0.02% (w/w) CA diets than that in the HFD group; on the other hand, the expression level of β-oxidation-related genes, such as peroxisome proliferator-activated receptor α (PPAR-α), carnitine palmitoyltransferase 1 (CPT-1), and acyl-CoA oxidase (ACO), was higher in mice fed a 0.02% (w/w) CA diet, than that in the HFD group (P < 0.05). In addition, the hepatic content of palmitic acid (C16:0), palmitoleic acid (C16:1), and oleic acid (C18:1) was significantly lower in mice fed the 0.02% (w/w) CA diet than that in the HFD group (P < 0.05). These results suggest that orally administered CA suppressed HFD-induced hepatic steatosis and fatty liver-related metabolic disorders through decrease of de novo lipogenesis and fatty acid elongation and increase of fatty acid β-oxidation in mice.
登录
查看更多内容
影响因子：
5.1
作者：
Manoharan, Shanmugam;VasanthaSelvan, MuthamizhSelvan;Kumar, Veerasamy Vinoth
通讯作者：
Kumar, Veerasamy Vinoth
CARD3 缺陷会加剧雄性小鼠饮食引起的肥胖、肝脂肪变性和胰岛素抵抗
影响因子：
4.8
作者：
Wang, Xin-An;Deng, Shan;Li, Hongliang
通讯作者：
Li, Hongliang
DOI：
10.1073/pnas.0904944106
发表时间：
2009-09-08
影响因子：
11.1
作者：
Fabbrini, Elisa;Magkos, Faidon;Klein, Samuel
通讯作者：
Klein, Samuel
影响因子：
13.5
作者：
Fabbrini, Elisa;Sullivan, Shelby;Klein, Samuel
通讯作者：
Klein, Samuel
影响因子：
13.5
作者：
Kleiner, DE;Brunt, EM;Sanyal, AJ
通讯作者：
Sanyal, AJ