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首页> 外文期刊>European journal of nutrition >Dietary intervention using (1,3)/(1,6)-beta-glucan, a fungus-derived soluble prebiotic ameliorates high-fat diet-induced metabolic distress and alters beneficially the gut microbiota in mice model
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Dietary intervention using (1,3)/(1,6)-beta-glucan, a fungus-derived soluble prebiotic ameliorates high-fat diet-induced metabolic distress and alters beneficially the gut microbiota in mice model

机译:使用(1,3)/(1,6)-beta-glucan,一种真菌衍生的可溶性益生菌改善高脂饮食诱导的代谢窘迫,并在小鼠模型中改变肠道微生物

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Purpose Western diet, rich in carbohydrates and fat, is said to be a major factor underlying metabolic syndrome. Interventions with prebiotics, the key modulators of the gut microbiota, have paramount impact on host-associated metabolic disorders. Herein, we investigated the effect of fungus-derived (1,3)/(1,6)-beta-glucan, a highly soluble dietary fiber, on high-fat diet (HFD)-induced metabolic distress. Methods Male C57BL/6 J mice were fed with different diet groups (n = 11): control diet, HFD, 3 g/kg or 5 g/kg of beta-glucan-incorporated HFD. At the end of experimental study period (12th week), body weight, feces weight and fecal moisture content were observed. Further, colonic motility was measured using activated charcoal meal study. Proteins extracted from liver and intestine tissues were subjected to western blot technique. Paraffin-embedded intestinal tissues were sectioned for histochemical [Periodic acid-Schiff (PAS) and Alcian blue (AB) staining] analysis. Fecal microbiota analysis was performed using MOTHUR bioinformatic software. Results beta-glucan consumption exhibited anti-obesity property in mice groups fed with HFD. In addition, beta-glucan ameliorated HFD-induced hepatic stress, colonic motility and intestinal atrophy (reduction in colon length, goblet cells, and mucosal layer thickness). Further, beta-glucan incorporation shifted bacterial community by increasing butyrate-producing bacteria such as Anaerostipes, Coprobacillus, and Roseburia and decreasing reportedly obesity-associated bacteria such as Parabacteroides and Lactococcus. Conclusion Altogether, the outcomes of this present pre-clinical animal study show beta-glucan to be a promising therapeutic candidate in the treatment of HFD-induced metabolic distress. Further comprehensive research has to be conducted to brace its clinical relevance, reproducibility and efficacy for aiding human health.
机译:目的西部饮食,富含碳水化合物和脂肪,据说是代谢综合征的主要因素。与益生元的干预肠道微生物群的关键调节剂,对宿主相关的代谢障碍具有最重要的影响。在此,我们研究了真菌衍生(1,3)/(1,6)-β-葡聚糖,高脂肪饮食(HFD)诱导的代谢窘迫的影响。方法将雄性C57BL / 6 J小鼠用不同的饮食组(n = 11):对照饮食,HFD,3g / kg或5g / kgβ-葡聚糖掺入的HFD。在实验研究期(第12周)结束时,观察到体重,粪便重量和粪便水分含量。此外,使用活性炭膳食研究测量结肠运动性。从肝脏和肠组织中提取的蛋白质进行Western印迹技术。分析组织化学[定期酸 - 席夫(PAS)和Alcian Blue(AB)染色]分析石蜡包埋肠组织。使用Mothur生物信息软件进行粪便微生物群分析。结果β-葡聚糖消耗表现出与HFD喂养的小鼠组中的抗肥胖性质。此外,β-葡聚糖改善了HFD诱导的肝脏应激,结肠运动性和肠道萎缩(降低结肠长度,脚杯细胞和粘膜层厚度)。此外,β-葡聚糖掺入通过增加丁酸丁酯,豆类植物和Roseburia等丁酸盐产生的细菌和据报道的肥胖相关细菌(如ParaMacteroides)和乳乳杆菌等抑制细菌群落。结论完全是,本发明前临床动物研究的结果显示β-葡聚糖是治疗HFD诱导的代谢窘迫的有希望的治疗候选者。必须进行进一步的综合研究,以满足其临床相关性,可重复性和疗效,以实现人类健康。

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