This study aimed to investigate the effects of β-glucan (LDBG) in preventing high-fat diet (HFD)-induced obesity in male C57BL/6 mice, focusing on fecal gut microbiota (GM) and plasma metabolomics. LDBG treatment led to a reduction in body weight and an improvement in dyslipidemia in the HFD-fed mice. Additionally, LDBG decreased pro-inflammatory factors (TNF-α, IL-1β, and IL-6) in liver and abdominal adipose tissue and lowered lipopolysaccharide and leptin levels in plasma. LDBG also up-regulated mRNA levels of intestinal epithelial tight junction proteins, such as Occludin, Claudin-1, and zonula occludens-1 in colon tissue. Furthermore, 16S rRNA gene sequencing data suggested that LDBG reduced the relative abundance of and while increasing that of and . Untargeted metabolomics showed that LDBG significantly promoted Tryptophan metabolism, Glycerophospholipid metabolism, and the Citrate cycle, closely correlating with GM changes, particularly in genera. This study demonstrates the potential of LDBG as a prebiotic in obesity prevention by regulating metabolite pathways.

中文翻译：

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来自 Lyophyllum decastes 的 β-葡聚糖调节高脂饮食诱导的肥胖小鼠的肠道微生物群和血浆代谢物


本研究旨在研究 β-葡聚糖 (LDBG) 在预防雄性 C57BL/6 小鼠高脂饮食 (HFD) 诱导的肥胖方面的作用，重点关注粪便肠道微生物群 (GM) 和血浆代谢组学。 LDBG 治疗导致 HFD 喂养的小鼠体重减轻并改善血脂异常。此外，LDBG 还能减少肝脏和腹部脂肪组织中的促炎因子（TNF-α、IL-1β 和 IL-6），并降低血浆中的脂多糖和瘦素水平。 LDBG 还上调结肠组织中肠上皮紧密连接蛋白（例如 Occludin、Claudin-1 和 zonula occlusionns-1）的 mRNA 水平。此外，16S rRNA基因测序数据表明，LDBG降低了 和 的相对丰度，同时增加了 和 的相对丰度。非靶向代谢组学表明，LDBG 显着促进色氨酸代谢、甘油磷脂代谢和柠檬酸循环，与 GM 变化密切相关，特别是在属中。这项研究证明了 LDBG 作为益生元通过调节代谢途径预防肥胖的潜力。