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      Phytochemicals That Influence Gut Microbiota as Prophylactics and for the Treatment of Obesity and Inflammatory Diseases

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          Abstract

          Gut microbiota (GM) plays several crucial roles in host physiology and influences several relevant functions. In more than one respect, it can be said that you “feed your microbiota and are fed by it.” GM diversity is affected by diet and influences metabolic and immune functions of the host's physiology. Consequently, an imbalance of GM, or dysbiosis, may be the cause or at least may lead to the progression of various pathologies such as infectious diseases, gastrointestinal cancers, inflammatory bowel disease, and even obesity and diabetes. Therefore, GM is an appropriate target for nutritional interventions to improve health. For this reason, phytochemicals that can influence GM have recently been studied as adjuvants for the treatment of obesity and inflammatory diseases. Phytochemicals include prebiotics and probiotics, as well as several chemical compounds such as polyphenols and derivatives, carotenoids, and thiosulfates. The largest group of these comprises polyphenols, which can be subclassified into four main groups: flavonoids (including eight subgroups), phenolic acids (such as curcumin), stilbenoids (such as resveratrol), and lignans. Consequently, in this review, we will present, organize, and discuss the most recent evidence indicating a relationship between the effects of different phytochemicals on GM that affect obesity and/or inflammation, focusing on the effect of approximately 40 different phytochemical compounds that have been chemically identified and that constitute some natural reservoir, such as potential prophylactics, as candidates for the treatment of obesity and inflammatory diseases.

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          Most cited references159

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          Flavonoids as antioxidants in plants: location and functional significance.

          Stress-responsive dihydroxy B-ring-substituted flavonoids have great potential to inhibit the generation of reactive oxygen species (ROS) and reduce the levels of ROS once they are formed, i.e., to perform antioxidant functions. These flavonoids are located within or in the proximity of centers of ROS generation in severely stressed plants. Efficient mechanisms have been recently identified for the transport of flavonoids from the endoplasmic reticulum, the site of their biosynthesis, to different cellular compartments. The mechanism underlying flavonoid-mediated ROS reduction in plants is still unclear. 'Antioxidant' flavonoids are found in the chloroplast, which suggests a role as scavengers of singlet oxygen and stabilizers of the chloroplast outer envelope membrane. Dihydroxy B-ring substituted flavonoids are present in the nucleus of mesophyll cells and may inhibit ROS-generation making complexes with Fe and Cu ions. The genes that govern the biosynthesis of antioxidant flavonoids are present in liverworts and mosses and are mostly up-regulated as a consequence of severe stress. This suggests that the antioxidant flavonoid metabolism is a robust trait of terrestrial plants. Vacuolar dihydroxy B-ring flavonoids have been reported to serve as co-substrates for vacuolar peroxidases to reduce H(2)O(2) escape from the chloroplast, following the depletion of ascorbate peroxidase activity. Antioxidant flavonoids may effectively control key steps of cell growth and differentiation, thus acting regulating the development of the whole plant and individual organs. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
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            How host-microbial interactions shape the nutrient environment of the mammalian intestine.

            Humans and other mammals are colonized by a vast, complex, and dynamic consortium of microorganisms. One evolutionary driving force for maintaining this metabolically active microbial society is to salvage energy from nutrients, particularly carbohydrates, that are otherwise nondigestible by the host. Much of our understanding of the molecular mechanisms by which members of the intestinal microbiota degrade complex polysaccharides comes from studies of Bacteroides thetaiotaomicron, a prominent and genetically manipulatable component of the normal human and mouse gut. Colonization of germ-free mice with B. thetaiotaomicron has shown how this anaerobe modifies many aspects of intestinal cellular differentiation/gene expression to benefit both host and microbe. These and other studies underscore the importance of understanding precisely how nutrient metabolism serves to establish and sustain symbiotic relationships between mammals and their bacterial partners.
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              The role of the gut microbiota in NAFLD.

              NAFLD is now the most common cause of liver disease in Western countries. This Review explores the links between NAFLD, the metabolic syndrome, dysbiosis, poor diet and gut health. Animal studies in which the gut microbiota are manipulated, and observational studies in patients with NAFLD, have provided considerable evidence that dysbiosis contributes to the pathogenesis of NAFLD. Dysbiosis increases gut permeability to bacterial products and increases hepatic exposure to injurious substances that increase hepatic inflammation and fibrosis. Dysbiosis, combined with poor diet, also changes luminal metabolism of food substrates, such as increased production of certain short-chain fatty acids and alcohol, and depletion of choline. Changes to the microbiome can also cause dysmotility, gut inflammation and other immunological changes in the gut that might contribute to liver injury. Evidence also suggests that certain food components and lifestyle factors, which are known to influence the severity of NAFLD, do so at least in part by changing the gut microbiota. Improved methods of analysis of the gut microbiome, and greater understanding of interactions between dysbiosis, diet, environmental factors and their effects on the gut-liver axis should improve the treatment of this common liver disease and its associated disorders.
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                Author and article information

                Contributors
                Journal
                Mediators Inflamm
                Mediators Inflamm
                MI
                Mediators of Inflammation
                Hindawi
                0962-9351
                1466-1861
                2018
                26 March 2018
                : 2018
                : 9734845
                Affiliations
                1Universidad de Guadalajara, Laboratorio de Ciencias de los Alimentos, Departamento de Reproducción Humana, Crecimiento y Desarrollo Infantil, CUCS, Guadalajara, JAL, Mexico
                2Universidad de Guadalajara, Laboratorio de Investigación y Desarrollo Farmacéutico, Departamento de Farmacobiología, CUCEI, Guadalajara, JAL, Mexico
                3Universidad Nacional Autónoma de México, Instituto Nacional de Pediatría, Unidad de Genética de la Nutrición, Instituto de Investigaciones Biomédicas, Mexico City, Mexico
                4Universidad de Guadalajara, Laboratorio de Neuroinmunobiología Molecular, Instituto de Investigación en Ciencias Biomédicas (IICB), CUCS, Guadalajara, JAL, Mexico
                5Universidad de Guadalajara, Laboratorio de Evaluación del Estado Nutricio, Departamento de Reproducción Humana, Crecimiento y Desarrollo Infantil, CUCS, Guadalajara, JAL, Mexico
                Author notes

                Academic Editor: Amedeo Amedei

                Author information
                http://orcid.org/0000-0003-1947-4276
                http://orcid.org/0000-0002-2339-4108
                http://orcid.org/0000-0001-8062-7118
                http://orcid.org/0000-0002-7443-2514
                Article
                10.1155/2018/9734845
                5896216
                29785173
                be13b068-5ca6-4279-8e97-801034744220
                Copyright © 2018 Lucrecia Carrera-Quintanar et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 15 September 2017
                : 17 January 2018
                : 13 February 2018
                Funding
                Funded by: CONACyT-México
                Award ID: 622462
                Award ID: CB-2015-256736
                Funded by: Universidad de Guadalajara
                Award ID: SEP-UDG-CA-454
                Award ID: PRO-SNI 2017
                Categories
                Review Article

                Immunology
                Immunology

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