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Insights into the role of gut microbiota in obesity: pathogenesis, mechanisms, and therapeutic perspectives

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      An obesity-associated gut microbiome with increased capacity for energy harvest.

      The worldwide obesity epidemic is stimulating efforts to identify host and environmental factors that affect energy balance. Comparisons of the distal gut microbiota of genetically obese mice and their lean littermates, as well as those of obese and lean human volunteers have revealed that obesity is associated with changes in the relative abundance of the two dominant bacterial divisions, the Bacteroidetes and the Firmicutes. Here we demonstrate through metagenomic and biochemical analyses that these changes affect the metabolic potential of the mouse gut microbiota. Our results indicate that the obese microbiome has an increased capacity to harvest energy from the diet. Furthermore, this trait is transmissible: colonization of germ-free mice with an 'obese microbiota' results in a significantly greater increase in total body fat than colonization with a 'lean microbiota'. These results identify the gut microbiota as an additional contributing factor to the pathophysiology of obesity.
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        A core gut microbiome in obese and lean twins

        The human distal gut harbors a vast ensemble of microbes (the microbiota) that provide us with important metabolic capabilities, including the ability to extract energy from otherwise indigestible dietary polysaccharides1–6. Studies of a small number of unrelated, healthy adults have revealed substantial diversity in their gut communities, as measured by sequencing 16S rRNA genes6–8, yet how this diversity relates to function and to the rest of the genes in the collective genomes of the microbiota (the gut microbiome) remains obscure. Studies of lean and obese mice suggest that the gut microbiota affects energy balance by influencing the efficiency of calorie harvest from the diet, and how this harvested energy is utilized and stored3–5. To address the question of how host genotype, environmental exposures, and host adiposity influence the gut microbiome, we have characterized the fecal microbial communities of adult female monozygotic and dizygotic twin pairs concordant for leanness or obesity, and their mothers. Analysis of 154 individuals yielded 9,920 near full-length and 1,937,461 partial bacterial 16S rRNA sequences, plus 2.14 gigabases from their microbiomes. The results reveal that the human gut microbiome is shared among family members, but that each person’s gut microbial community varies in the specific bacterial lineages present, with a comparable degree of co-variation between adult monozygotic and dizygotic twin pairs. However, there was a wide array of shared microbial genes among sampled individuals, comprising an extensive, identifiable ‘core microbiome’ at the gene, rather than at the organismal lineage level. Obesity is associated with phylum-level changes in the microbiota, reduced bacterial diversity, and altered representation of bacterial genes and metabolic pathways. These results demonstrate that a diversity of organismal assemblages can nonetheless yield a core microbiome at a functional level, and that deviations from this core are associated with different physiologic states (obese versus lean).
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          Microbial ecology: human gut microbes associated with obesity.

          Two groups of beneficial bacteria are dominant in the human gut, the Bacteroidetes and the Firmicutes. Here we show that the relative proportion of Bacteroidetes is decreased in obese people by comparison with lean people, and that this proportion increases with weight loss on two types of low-calorie diet. Our findings indicate that obesity has a microbial component, which might have potential therapeutic implications.
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            Author and article information

            Affiliations
            [1 ]ISNI 0000 0004 1761 4404, GRID grid.233520.5, State Key Laboratory of Cancer Biology & Institute of Digestive Diseases Xijing Hospital, , The Fourth Military Medical University, ; Xi’an, 710032 China
            [2 ]ISNI 0000 0004 1761 4404, GRID grid.233520.5, Department of Clinical Nutrition, Xi Jing Hospital, , The Fourth Military Medical University, ; Xi’an, 710032 China
            [3 ]ISNI 0000 0001 2256 9319, GRID grid.11135.37, Department of Dermatology and Venereology, Peking University First Hospital, Research Center for Medical Mycology, , Peking University, ; Beijing, 100034 China
            [4 ]GRID grid.452511.6, Medical Center for Digestive Diseases, , The Second Affiliated Hospital of Nanjing Medical University, ; Nanjing, 210001 China
            Contributors
            86-29-84771620 , yongznie@fmmu.edu.cn
            Journal
            Protein Cell
            Protein Cell
            Protein & Cell
            Higher Education Press (Beijing )
            1674-800X
            1674-8018
            3 May 2018
            3 May 2018
            May 2018
            : 9
            : 5
            : 397-403
            29725936 5960470 546 10.1007/s13238-018-0546-3
            © The Author(s) 2018

            Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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.

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            © HEP and Springer-Verlag GmbH Germany, part of Springer Nature 2018

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