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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/81171

    Title: Asiatic acid ameliorates hepatic lipid accumulation and insulin resistance in mice consuming high fat diet
    Authors: Ya, Sheng-lei;Yan, Sheng-lei;Yan, Hui-ting;Yang, Hui-ting;Lee, Yi-ju;Lee, Yi-ju;Lin, Chun-che;Lin, Chun-che;Cha, Ming-hui;Chang, Ming-hui;殷梅津*
    Contributors: 保健營養生技學系
    Keywords: asiatic acid;high-fat diet;hepatic steatosis;insulin resistance
    Date: 2014-05
    Issue Date: 2014-10-01 16:48:59 (UTC+8)
    Abstract: Effects of asiatic acid (AA) at 10 or 20 mg/kg/day upon hepatic steatosis in mice consuming a high-fat diet (HFD) were examined. AA intake decreased body weight, water intake, feed intake, epididymal fat, and plasma and hepatic triglyceride levels in HFD-treated mice (P < 0.05). HFD enhanced 2.85-fold acetyl coenzyme A carboxylase (ACC1), 3.34-fold fatty acid synthase (FAS), 3.71-fold stearoyl CoA desaturase (SCD)-1, 3.62-fold 3-hydroxy-3-methylglutaryl coenzyme A reductase, 2.91-fold sterol regulatory element-binding protein (SREBP)-1c, and 2.75-fold SREBP-2 expression in liver (P < 0.05). Compared with HFD groups, AA intake at two doses reduced 18.9-45.7% ACC1, 25.1-49.8% FAS, 24.7-57.1% SCD-1, and 21.8-53.3% SREBP-1c protein expression (P < 0.05). Histological results indicated AA intake at two doses reduced hepatic lipid accumulation and inflammatory infiltrate. HFD increased hepatic production of reactive oxygen species, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, as well as decreased hepatic glutathione content and glutathione peroxidase and catalase activities (P < 0.05). AA intake at two doses reversed these alterations (P < 0.05). AA intake suppressed 32.4-58.8% nuclear factor kappa (NF-κ)B p65 and 24.2-56.7% p-p38 expression (P < 0.05) and at high dose down-regulated 29.1% NF-κB p50 and 40.7% p-JNK expression in livers from HFD-treated mice. AA intake at two doses lowered plasma insulin secretion and HOMR-IR (P < 0.05). These results suggest that AA is a potent hepatic protective agent against HFD-induced hepatic injury.
    Appears in Collections:[食品營養與保健生技學系] 期刊論文

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