首页> 外文期刊>The Journal of Nutritional Biochemistry >Altered mRNA expression of hepatic lipogenic enzyme and PPARalpha in rats fed dietary levan from Zymomonas mobilis
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Altered mRNA expression of hepatic lipogenic enzyme and PPARalpha in rats fed dietary levan from Zymomonas mobilis

机译:运动发酵单胞菌饮食饲料喂养大鼠肝脏脂肪酶和PPARαmRNA表达的变化。

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Levan or high molecular beta-2,6-linked fructose polymer is produced extracellularly from sucrose-based substrates by bacterial levansucrase. In the present study, to investigate the effect of levan feeding on serum leptin, hepatic lipogenic enzyme and peroxisome proliferation-activated receptor (PPAR) alpha expression in high-fat diet-induced obese rats, 4-week-old Sprague-Dawley male rats were fed high-fat diet (beef tallow, 40% of calories as fat), and, 6 weeks later, the rats were fed 0%, 1%, 5% or 10% levan-supplemented diets for 4 weeks. Serum leptin and insulin level were dose dependently reduced in levan-supplemented diet-fed rats. The mRNA expressions of hepatic fatty acid synthase and acetyl CoA carboxylase, which are the key enzymes in fatty acid synthesis, were down-regulated by dietary levan. However, dietary levan did not affect the gene expression of hepatic malic enzyme, phosphatidate phosphohydrolase and HMG CoA reductase. Also, the lipogenic enzyme gene expression in the white adipose tissue (WAT) was not affected by the diet treatments. However, hepatic PPARalpha mRNA expression was dose dependently up-regulated by dietary levan, whereas PPARgamma in the WAT was not changed. The results suggest that the in vivo hypolipidemic effect of dietary levan, including anti-obesity and lipid-lowering, may result from the inhibition of lipogenesis and stimulation of lipolysis, accompanied with regulation of hepatic lipogenic enzyme and PPARalpha gene expression.
机译:Levan或高分子β-2,6-连接的果糖聚合物是由细菌蔗糖酶从蔗糖基底物胞外产生的。在本研究中,为了研究levan喂养对高脂饮食诱导的肥胖大鼠,4周龄Sprague-Dawley雄性大鼠血清瘦素,肝脂肪酶和过氧化物酶体增殖激活受体(PPAR)α表达的影响饲喂高脂饮食(牛脂,40%的卡路里以脂肪计),并在6周后给大鼠饲喂0%,1%,5%或10%的Levan补充饮食,持续4周。在补充有饮食的大鼠中,血清瘦素和胰岛素水平呈剂量依赖性降低。饮食中levan下调了脂肪酸合成中的关键酶-肝脂肪酸合酶和乙酰辅酶A羧化酶的mRNA表达。但是,饮食中的莱万不影响肝苹果酸酶,磷脂酸磷酸水解酶和HMG CoA还原酶的基因表达。而且,白色脂肪组织(WAT)中的脂肪生成酶基因表达不受饮食治疗的影响。但是,肝中PPARalpha mRNA的表达受饮食水平的剂量依赖性上调,而WAT中的PPARgamma却没有改变。结果表明,饮食脂肪的体内降血脂作用,包括抗肥胖和降脂,可能是由于抑制脂肪生成和刺激脂肪分解,以及调节肝脏脂肪生成酶和PPARalpha基因表达而引起的。

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