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dfa1 在高脂诱导肥胖小鼠的抗肥胖方面优于 dfa1,可能是通过在肠道菌群失调缓解方面的差异,尽管它们具有相似的抗炎特性。

dfa1 Outperforms dfa1 on Anti-Obesity in High Fat-Induced Obesity Mice Possibly through the Differences in Gut Dysbiosis Attenuation, despite the Similar Anti-Inflammatory Properties.

机构信息

Department of Preventive and Social Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.

Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.

出版信息

Nutrients. 2021 Dec 25;14(1):80. doi: 10.3390/nu14010080.

Abstract

Fat reduction and anti-inflammation are commonly claimed properties of probiotics. and were tested in high fat-induced obesity mice and in vitro experiments. After 16 weeks of probiotics, dfa1 outperforms dfa1 on the anti-obesity property as indicated by body weight, regional fat accumulation, serum cholesterol, inflammatory cytokines (in blood and colon tissue), and gut barrier defect (FITC-dextran assay). With fecal microbiome analysis, dfa1 but not dfa1 reduced fecal abundance of pathogenic Proteobacteria without an alteration in total Gram-negative bacteria when compared with non-probiotics obese mice. With palmitic acid induction, the condition media from both probiotics similarly attenuated supernatant IL-8, improved enterocyte integrity and down-regulated cholesterol absorption-associated genes in Caco-2 cell (an enterocyte cell line) and reduced supernatant cytokines (TNF-α and IL-6) with normalization of cell energy status (extracellular flux analysis) in bone-marrow-derived macrophages. Due to the anti-inflammatory effect of the condition media of both probiotics on palmitic acid-activated enterocytes was neutralized by amylase, the active anti-inflammatory molecules might, partly, be exopolysaccharides. As dfa1 out-performed dfa1 in anti-obesity property, possibly through the reduced fecal Proteobacteria, with a similar anti-inflammatory exopolysaccharide; is a potentially better option for anti-obesity than .

摘要

减肥和抗炎是益生菌的常见特性。我们在高脂肪诱导的肥胖小鼠和体外实验中测试了和。经过 16 周的益生菌治疗,与非益生菌肥胖小鼠相比,dfa1 在减肥特性上优于 dfa1,表现为体重、局部脂肪堆积、血清胆固醇、炎症细胞因子(血液和结肠组织)和肠道屏障缺陷(FITC-葡聚糖测定)。通过粪便微生物组分析,dfa1 而非 dfa1 降低了粪便中致病性变形菌的丰度,而总革兰氏阴性菌没有改变。用棕榈酸诱导时,两种益生菌的条件培养基均相似地减弱了上清液中 IL-8 的含量,改善了 Caco-2 细胞(肠上皮细胞系)中肠上皮细胞的完整性,并下调了胆固醇吸收相关基因,同时在骨髓来源的巨噬细胞中恢复细胞能量状态(细胞外通量分析),降低上清液中的细胞因子(TNF-α 和 IL-6)。由于两种益生菌的条件培养基对棕榈酸激活的肠上皮细胞的抗炎作用被淀粉酶中和,因此,活性抗炎分子可能部分是胞外多糖。由于 dfa1 在减肥特性上优于 dfa1,可能是通过减少粪便变形菌,同时具有相似的抗炎胞外多糖;因此,与相比,是一种更有潜力的减肥益生菌。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a37/8746774/433c9fcb5e5d/nutrients-14-00080-g001.jpg

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