共查询到20条相似文献,搜索用时 15 毫秒
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Inés Martínez James M Lattimer Kelcie L Hubach Jennifer A Case Junyi Yang Casey G Weber Julie A Louk Devin J Rose Gayaneh Kyureghian Daniel A Peterson Mark D Haub Jens Walter 《The ISME journal》2013,7(2):269-280
The involvement of the gut microbiota in metabolic disorders, and the ability of whole grains to affect both host metabolism and gut microbial ecology, suggest that some benefits of whole grains are mediated through their effects on the gut microbiome. Nutritional studies that assess the effect of whole grains on both the gut microbiome and human physiology are needed. We conducted a randomized cross-over trial with four-week treatments in which 28 healthy humans consumed a daily dose of 60 g of whole-grain barley (WGB), brown rice (BR), or an equal mixture of the two (BR+WGB), and characterized their impact on fecal microbial ecology and blood markers of inflammation, glucose and lipid metabolism. All treatments increased microbial diversity, the Firmicutes/Bacteroidetes ratio, and the abundance of the genus Blautia in fecal samples. The inclusion of WGB enriched the genera Roseburia, Bifidobacterium and Dialister, and the species Eubacterium rectale, Roseburia faecis and Roseburia intestinalis. Whole grains, and especially the BR+WGB treatment, reduced plasma interleukin-6 (IL-6) and peak postprandial glucose. Shifts in the abundance of Eubacterium rectale were associated with changes in the glucose and insulin postprandial response. Interestingly, subjects with greater improvements in IL-6 levels harbored significantly higher proportions of Dialister and lower abundance of Coriobacteriaceae. In conclusion, this study revealed that a short-term intake of whole grains induced compositional alterations of the gut microbiota that coincided with improvements in host physiological measures related to metabolic dysfunctions in humans. 相似文献
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Man Wang Fei Yu Yuan Zhang Wenguang Chang Meng Zhou 《International journal of biological sciences》2022,18(4):1451
Flavonoids are a group of polyphenolic compounds which are ubiquitously found in plants and are consumed as part of the human diet in substantial amounts. The verification of flavonoids'' cancer chemopreventive benefits has led to a significant interest in this field. Gut microbiota includes a diverse community of microorganisms and has a close relationship with cancer development. Increasing evidence has indicated that flavonoids exert anticarcinogenic effects by reshaping gut microbiota. Gut microbiota can convert flavonoids into bioactive metabolites that possess anticancer activity. Here, we present a brief introduction to gut microbiota and provide an overview of the interplay between gut microbiota and cancer pathogenesis. We also highlight the crucial roles of flavonoids in preventing cancer based on their regulation of gut microbiota. This review would encourage research on the flavonoid-intestinal microbiota interactions and clinical trials to validate the chemotherapeutic potentials of targeting gut microbiota by dietary bioactive compounds. 相似文献
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观察应激性高血压大鼠肠道菌群的变化,探索肠道菌群在应激性高血压发生中的作用。应激性高血压模型的制备:大鼠每天2次接受足底电刺激加噪声的应激,每次2 h,中间间隔4 h,共14 d。血压的测量:大鼠股动脉插管,Powerlab系统记录血压。伪无菌鼠的制备:在大鼠的饮用水中加入氨苄西林(1 g/L)、万古霉素(500 mg/L)、新霉素(1 g/L)和甲硝唑(1 g/L)4种抗生素,共持续4周。采用Illumina MiSeq测序技术,测定大鼠粪便中微生物16S rRNA V3-V4区序列,并对群落结构和多样性进行比较分析。慢性应激导致大鼠血压升高,心率加快,血清去甲肾上腺素浓度增加;α多样性分析显示应激大鼠肠道菌群丰富度和多样性下降,β多样性分析显示应激组大鼠肠道菌群物种组成变少,差异性变大;伪无菌鼠的肠道菌群物种单一,仅有少量的变形菌门。给予伪无菌鼠相同的慢性应激,不能引起大鼠血压升高、心率增快,血清去甲肾上腺素浓度未升高。应激引起大鼠肠道菌群紊乱,应激性高血压的发生可能依赖于肠道菌群的状态。 相似文献
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肠道菌群与能量代谢密切相关,其组成和代谢紊乱可通过多种途径导致胰岛素抵抗,肥胖和2型糖尿病。黄连素因具有减重、降糖、调脂等作用被广泛用于肥胖、2型糖尿病及非酒精性脂肪性肝病等代谢性疾病的辅助治疗;研究表明,黄连素可调节肠道菌群的组成和代谢,改善肠道微生态环境,从而改善胰岛素抵抗和代谢。本文综述了黄连素通过肠道菌群-炎症轴在干预代谢性疾病的研究进展,以期为代谢性疾病的治疗寻找新的策略,并为今后该领域的深入研究提供指导意义。 相似文献
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目的:研究两种不同植物甾醇酯对高脂血症大鼠的降血脂作用,并比较其差异。方法:通过饲喂高脂饲料,建立高脂血症大鼠模型,将建模成功的大鼠,按照TC水平随机分成8组,即模型对照组,溶剂对照组,Vegapure 95FF低、中、高剂量组,Vegapure 95E低、中、高剂量组,同时设立空白对照组。干预4周后,记录体重、进食量,并检测血清TC、LDL-C、TG、HDL-C、脂肪重量及体脂率、肝脏重量及肝脏指数等指标。结果:在实验剂量下,两种植物甾醇酯均明显降低血清TC、LDL-C,但均未发现有剂量效应关系;两种植物甾醇酯对血清TG、HDL-C无明显影响。两种植物甾醇酯对高脂血症SD大鼠体重增长、进食量、脂肪重量、体脂率、肝脏重量和肝脏指数均无明显影响。结论:两种植物甾醇酯在降低血脂、大鼠生长发育、体质和肝脏方面均无明显差异。 相似文献
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Mingyue Li Weina Guo Yalan Dong Wenzhu Wang Chunxia Tian Zili Zhang Ting Yu Haifeng Zhou Yang Gui Kaming Xue Junyi Li Feng Jiang Alexey Sarapultsev Huafang Wang Ge Zhang Shanshan Luo Heng Fan Desheng Hu 《基因组蛋白质组与生物信息学报(英文版)》2022,20(2):288-303
Ulcerative colitis (UC) is a chronic inflammatory bowel disease caused by many factors including colonic inflammation and microbiota dysbiosis. Previous studies have indicated that celastrol (CSR) has strong anti-inflammatory and immune-inhibitory effects. Here, we investigated the effects of CSR on colonic inflammation and mucosal immunity in an experimental colitis model, and addressed the mechanism by which CSR exerts the protective effects. We characterized the therapeutic effects and the potential mechanism of CSR on treating UC using histological staining, intestinal permeability assay, cytokine assay, flow cytometry, fecal microbiota transplantation (FMT), 16S rRNA sequencing, untargeted metabolomics, and cell differentiation. CSR administration significantly ameliorated the dextran sodium sulfate (DSS)-induced colitis in mice, which was evidenced by the recovered body weight and colon length as well as the decreased disease activity index (DAI) score and intestinal permeability. Meanwhile, CSR down-regulated the production of pro-inflammatory cytokines and up-regulated the amount of anti-inflammatory mediators at both mRNA and protein levels, and improved the balances of Treg/Th1 and Treg/Th17 to maintain the colonic immune homeostasis. Notably, all the therapeutic effects were exerted in a gut microbiota-dependent manner. Furthermore, CSR treatment increased the gut microbiota diversity and changed the compositions of the gut microbiota and metabolites, which is probably associated with the gut microbiota-mediated protective effects. In conclusion, this study provides the strong evidence that CSR may be a promising therapeutic drug for UC. 相似文献
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Seok-Won Kim Wataru Suda Sangwan Kim Kenshiro Oshima Shinji Fukuda Hiroshi Ohno Hidetoshi Morita Masahira Hattori 《DNA research》2013,20(3):241-253
Probiotics are live microorganisms that potentially confer beneficial outcomes to host by modulating gut microbiota in the intestine. The aim of this study was to comprehensively investigate effects of probiotics on human intestinal microbiota using 454 pyrosequencing of bacterial 16S ribosomal RNA genes with an improved quantitative accuracy for evaluation of the bacterial composition. We obtained 158 faecal samples from 18 healthy adult Japanese who were subjected to intervention with 6 commercially available probiotics containing either Bifidobacterium or Lactobacillus strains. We then analysed and compared bacterial composition of the faecal samples collected before, during, and after probiotic intervention by Operational taxonomic units (OTUs) and UniFrac distances. The results showed no significant changes in the overall structure of gut microbiota in the samples with and without probiotic administration regardless of groups and types of the probiotics used. We noticed that 32 OTUs (2.7% of all analysed OTUs) assigned to the indigenous species showed a significant increase or decrease of ≥10-fold or a quantity difference in >150 reads on probiotic administration. Such OTUs were found to be individual specific and tend to be unevenly distributed in the subjects. These data, thus, suggest robustness of the gut microbiota composition in healthy adults on probiotic administration. 相似文献
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An increasing number of studies have revealed an interaction between gut microbiota and tumors. The enrichment of specific bacteria strains in the intestines has been found to modulate tumor growth and influence the mechanisms of tumor treatment. Various bacteria are involved in modulating the effects of chemotherapeutic drugs currently used to treat patients with cancer, and they affect not only gastrointestinal tract tumors but also distant organ tumors. In addition, changes in the gut microbiota are known to be involved in the antitumor immune response as well as the modulation of the intestinal immune system. As a result, the gut microbiota plays an important role in modulating the efficacy of immune checkpoint inhibitors. Therefore, gut microbiota could be considered as an adjuvant treatment option with other cancer treatment or as another marker for predicting treatment response. In this review, we examine how gut microbiota affects cancer treatments. 相似文献
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《Cell reports》2020,30(11):3682-3690.e6
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Matteo Serino 《Journal of molecular biology》2018,430(5):581-590
Alterations of both ecology and functions of gut microbiota are conspicuous traits of several inflammatory pathologies, notably metabolic diseases such as obesity and type 2 diabetes. Moreover, the proliferation of enterobacteria, subdominant members of the intestinal microbial ecosystem, has been shown to be favored by Western diet, the strongest inducer of both metabolic diseases and gut microbiota dysbiosis. The inner interdependence between the host and the gut microbiota is based on a plethora of molecular mechanisms by which host and intestinal microbes modify each other. Among these mechanisms are as follows: (i) the well-known metabolic impact of short chain fatty acids, produced by microbial fermentation of complex carbohydrates from plants; (ii) a mutual modulation of miRNAs expression, both on the eukaryotic (host) and prokaryotic (gut microbes) side; (iii) the production by enterobacteria of virulence factors such as the genotoxin colibactin, shown to alter the integrity of host genome and induce a senescence-like phenotype in vitro; (iv) the microbial excretion of outer-membrane vesicles, which, in addition to other functions, may act as a carrier for multiple molecules such as toxins to be delivered to target cells. In this review, I describe the major molecular mechanisms by which gut microbes exert their metabolic impact at a multi-organ level (the gut barrier being in the front line) and support the emerging triad of metabolic diseases, gut microbiota dysbiosis and enterobacteria infections. 相似文献
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Breast cancer (BC) and benign breast lesions (BBLs) are common diseases in women worldwide. The gut microbiota plays a vital role in regulating breast diseases’ formation, progression, and therapy response. Hence, we explored the structure and function of gut microflora in patients with BC and BBLs. A cohort of 66 subjects was enrolled in the study. Twenty-six subjects had BC, 20 subjects had BBLs, and 20 matched healthy controls. High throughput 16S ribosomal RNA (16S rRNA) gene sequencing technology was used to determine the microbial community structure. Compared with healthy individuals, BC patients had significantly lower alpha diversity indices (Sobs index, p = 0.019; Chao1 index, p = 0.033). Sobs and Chao1 indices were also lower in patients with BBLs than healthy individuals, without statistical significance (p = 0.279, p = 0.314, respectively). Both unweighted and weighted UniFrac analysis showed that beta diversity differed significantly among the three groups (p = 3.376e–14, p < 0.001, respectively). Compared with healthy individuals, the levels of Porphyromonas and Peptoniphilus were higher in BC patients (p = 0.004, p = 0.007, respectively), whereas Escherichia and Lactobacillus were more enriched in the benign breast lesion group (p < 0.001, p = 0.011, respectively). Our study indicates that patients with BC and BBLs may undergo significant changes in intestinal microbiota. These findings can help elucidate the role of intestinal flora in BC and BBLs patients. Open in a separate window 相似文献