Consumption of barley β-glucan ameliorates fatty liver and insulin resistance in mice fed a high-fat diet
Consumption of barley β-glucan ameliorates fatty liver and insulin resistance in mice fed a high-fat diet
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DOI：
10.1002/mnfr.200900127
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发表时间：
2010-07-01
影响因子：
5.2
通讯作者：
Song, Jihyun
中科院分区：
文献类型：
--
作者：
Choi, Joo Sun;Kim, Hyunsook;Song, Jihyun
研究表明，食用富含大麦β-葡聚糖(BG)的饮食可以预防胰岛素抵抗。为探讨大麦BG的作用机制，将3组7周龄雄性C57BL/6J小鼠分别饲喂含0、2、4%大麦BG的高脂饲料12wk。与0%BG组相比，2%BG组和4%BG组的体重显著降低。4%BG组表现出糖耐量改善，胰岛素抵抗指数和葡萄糖依赖的胰岛素依赖型多肽水平降低。摄入BG饮食可降低肝脏脂肪含量。BG饮食的小鼠也表现出脂肪酸合成酶的降低和胆固醇7α-羟基酶基因表达水平的提高。BG饮食通过降低胰岛素受体底物1丝氨酸磷酸化和激活Akt来促进肝脏胰岛素信号转导，并降低葡萄糖-6-磷酸酶和磷酸烯醇式丙酮酸羧酸激酶的mRNA水平。总之，摄入BG减少了体重增加，减少了肝脏脂肪堆积，并改善了高脂饮食小鼠的胰岛素敏感性。BG摄入改变了糖脂代谢基因的表达，导致胰岛素信号转导增强。摄入大麦BG可能是预防肥胖、胰岛素抵抗和代谢综合征的有效策略。
Consumption of a diet high in barley beta-glucan (BG) has been shown to prevent insulin resistance. To investigate the mechanism for the effects of barley BG, three groups of male 7-wk-old C57BL/6J mice were fed high-fat diets containing 0, 2, or 4% of barley BG for 12 wk. The 2% BG and 4% BG groups had significantly lower body weights compared with the 0% BG group. The 4% BG group demonstrated improved glucose tolerance and lower levels of insulin-resistance index and glucose-dependent insulinotropic polypeptide. Consumption of the BG diet decreased hepatic lipid content. Mice on the BG diet also demonstrated decreased fatty acid synthase and increased cholesterol 7 alpha-hydroxylase gene expression levels. The BG diet promoted hepatic insulin signaling by decreasing serine phosphorylation of insulin receptor substrate 1 and activating Akt, and it decreased mRNA levels of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. In summary, consumption of BG reduced weight gain, decreased hepatic lipid accumulation, and improved insulin sensitivity in mice fed a high-fat diet. Insulin signaling enhanced due to the expression changes of glucose and lipid metabolism genes by BG consumption. Consumption of barley BG could be an effective strategy for preventing obesity, insulin resistance, and the metabolic syndrome.