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      Effect of coffee or coffee components on gut microbiome and short-chain fatty acids in a mouse model of metabolic syndrome

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          Abstract

          We previously showed that male Tsumura Suzuki obese diabetes (TSOD) mice, a spontaneous mouse model of metabolic syndrome, manifested gut dysbiosis and subsequent disruption of the type and quantity of plasma short-chain fatty acids (SCFAs), and daily coffee intake prevented nonalcoholic steatohepatitis in this mouse model. Here, we present a preliminary study on whether coffee and its major components, caffeine and chlorogenic acid, would affect the gut dysbiosis and the disrupted plasma SCFA profile of TSOD mice, which could lead to improvement in the liver pathology of these mice. Three mice per group were used. Daily intake of coffee or its components for 16 wk prevented liver lobular inflammation without improving obesity in TSOD mice. Coffee and its components did not repair the altered levels of Gram-positive and Gram-negative bacteria and an increased abundance of Firmicutes in TSOD mice but rather caused additional changes in bacteria in six genera. However, caffeine and chlorogenic acid partially improved the disrupted plasma SCFA profile in TSOD mice, although coffee had no effects. Whether these alterations in the gut microbiome and the plasma SCFA profile might affect the liver pathology of TSOD mice may deserve further investigation.

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          Gut microbiome, obesity, and metabolic dysfunction.

          The prevalence of obesity and related disorders such as metabolic syndrome has vastly increased throughout the world. Recent insights have generated an entirely new perspective suggesting that our microbiota might be involved in the development of these disorders. Studies have demonstrated that obesity and metabolic syndrome may be associated with profound microbiotal changes, and the induction of a metabolic syndrome phenotype through fecal transplants corroborates the important role of the microbiota in this disease. Dietary composition and caloric intake appear to swiftly regulate intestinal microbial composition and function. As most findings in this field of research are based on mouse studies, the relevance to human biology requires further investigation.
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            Gut microbiome composition is linked to whole grain-induced immunological improvements.

            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.
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              Probiotics, Prebiotics and Immunomodulation of Gut Mucosal Defences: Homeostasis and Immunopathology

              Probiotics are beneficial microbes that confer a realistic health benefit on the host, which in combination with prebiotics, (indigestible dietary fibre/carbohydrate), also confer a health benefit on the host via products resulting from anaerobic fermentation. There is a growing body of evidence documenting the immune-modulatory ability of probiotic bacteria, it is therefore reasonable to suggest that this is potentiated via a combination of prebiotics and probiotics as a symbiotic mix. The need for probiotic formulations has been appreciated for the health benefits in “topping up your good bacteria” or indeed in an attempt to normalise the dysbiotic microbiota associated with immunopathology. This review will focus on the immunomodulatory role of probiotics and prebiotics on the cells, molecules and immune responses in the gut mucosae, from epithelial barrier to priming of adaptive responses by antigen presenting cells: immune fate decision—tolerance or activation? Modulation of normal homeostatic mechanisms, coupled with findings from probiotic and prebiotic delivery in pathological studies, will highlight the role for these xenobiotics in dysbiosis associated with immunopathology in the context of inflammatory bowel disease, colorectal cancer and hypersensitivity.
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                Author and article information

                Contributors
                tsuneyama.koichi@tokushima-u.ac.jp
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                1 November 2018
                1 November 2018
                2018
                : 8
                : 16173
                Affiliations
                [1 ]ISNI 0000 0001 1092 3579, GRID grid.267335.6, Department of Pathology and Laboratory Medicine, Graduate School of Biomedical Sciences, , Tokushima University, ; 3-18-15 Kuramoto-cho, Tokushima, 770-8503 Japan
                [2 ]ISNI 0000 0004 1763 1087, GRID grid.412857.d, Department of Biochemistry, , Wakayama Medical University, ; 811-1 Kimiidera, Wakayama, 641-8509 Japan
                [3 ]ISNI 0000 0000 8801 3092, GRID grid.419972.0, Next Generation Science Institute, , Morinaga Milk Industry Co., Ltd., ; 5-1-83 Higashihara, Zama, Kanagawa 252-8583 Japan
                [4 ]ISNI 0000 0000 8863 9909, GRID grid.262576.2, Laboratory of Clinical and Analytical Chemistry, College of Pharmaceutical Sciences, , Ritsumeikan University, ; 1-1-1 Nojihigashi, Kusatsu, Shiga 525-8577 Japan
                [5 ]ISNI 0000 0001 1092 3579, GRID grid.267335.6, Education Support Room for Anatomy, , Tokushima University, ; 3-18-15 Kuramoto-cho, Tokushima, 770-8503 Japan
                [6 ]ISNI 0000 0001 0728 1069, GRID grid.260433.0, Department of Medicine for Aging in Place and Community-Based Medical Education, , Nagoya City University, Graduate School of Medical Sciences, ; 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi 467-8601 Japan
                Article
                34571
                10.1038/s41598-018-34571-9
                6212590
                30385796
                ac50a631-8e5b-49bc-a2ad-b97dd8c35d97
                © The Author(s) 2018

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 3 January 2018
                : 8 October 2018
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100001691, Japan Society for the Promotion of Science (JSPS);
                Award ID: 24390181
                Award ID: 25340121
                Award ID: 15K15098
                Award Recipient :
                Funded by: A Research grant of 2012 and 2015 from the All Japan Coffee Association.
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