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      Artificial sweeteners are not sweet to the gut microbiome

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      Genes & Diseases
      Chongqing Medical University

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          Abstract

          Most cells in our body are not human, but microbial; the ratio of ‘them’ to ‘us’ is about 10:1. 1 Perturbations of host-microbe interactions can lead to miscues and altered host responses that increase the risk of pathogenic processes and promote “western” disorders, such as obesity, diabetes, cancers, allergies, autism, asthma and inflammatory bowel diseases.2, 3 In theory, dietary components can affect the equilibrium between intestinal microbes and the host, leading to altered physiology. A recent report in Nature 4 provides additional evidence to support this theory, where it was found that the use of artificial sweeteners enhanced the risk of glucose intolerance in both mice and humans by altering the composition and behavior of the intestinal microbiota. Notably, changes of the bacterial Taxa (an over-representation of Bacteroides and an under-representation of Clostridiales) following the consumption of artificial sweeteners was previously found to be associated with type 2 diabetes 4 and other chronic diseases. 6 This study in Nature 4 provides a plausible explanation for the link between human health and the changing diet, demonstrated through a unique mechanism that shows how the use of artificial sweeteners impacts the host physiology and metabolism and decreases beneficial bacterial species, thus increasing the risk for obesity and type 2 diabetes in genetically susceptible hosts. These findings are relevant to many complex disorders, as well as other “new age” disorders, such as inflammatory bowel diseases, diabetes, metabolic syndrome and cancers, where the disturbed relationships among the lifestyle, genetics and the enteric microbiota have been implicated. The study by Suez, et al 4 helps to explain the upward trend in complex disorders, such as obesity, diabetes, allergy, and asthma, over the past half century, which may be related to changes in the diet, lifestyle [such as less outdoor activity (sun exposure) and more time indoors], and the human microbiomes that negatively impact individuals with genetic susceptibility. The public is aware of the alarming trends in diseases such as obesity, diabetes, inflammatory/immune disorders, and cancer. Many people are sensitive to the notion that these diseases are the consequences of our changing environment, diet and lifestyle. What the public wants to know is what factors cause these diseases, and how they can make changes to prevent/treat these conditions. The recent findings linking artificial sweeteners to dysbiosis and metabolic abnormalities call for a reassessment of the massive use of artificial sweeteners. This is because the diet can rapidly modulate the gut microbiota, 5 and alterations in the microbiota exert profound effects on the host physiology and metabolism. These findings may serve as a basis for personalized nutrition strategies to restore the microbial states associated with health. The enteric microbiota is malleable. However, we have realized that reaching for the high-hanging fruit, where biomedical discoveries related to the microbiome lie, requires a multi-disciplinary team effort from basic, translational, and clinical investigators and close attention to the current public health challenges.

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          Who are we? Indigenous microbes and the ecology of human diseases.

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            Exploring gut microbes in human health and disease: Pushing the envelope

            Humans have coevolved with their microbes over thousands of years, but this relationship, is now being dramatically affected by shifts in the collective human microbiome resulting from changes in the environment and societal norms. Resulting perturbations of intestinal host-microbe interactions can lead to miscues and altered host responses that increase the risk of pathogenic processes and promote “western” disorders such as inflammatory bowel diseases, cancers, obesity, diabetes, autism, and asthma. Given the current challenges and limitations in gene therapy, approaches that can reshape the gut microbiome represent a reasonable strategy for restoring the balance between host and microbes. In this review and commentary, we highlight recent progress in our understanding of the intestinal microbiome in the context of health and diseases, focusing on mechanistic concepts that underlie the complex relationships between host and microbes. Despite these gains, many challenges lie ahead that make it difficult to close the gap between the basic sciences and clinical application. We will discuss the potential therapeutic strategies that can be used to manipulate the gut microbiota, recognizing that the promise of pharmabiotics (“bugs to drugs”) is unlikely to be completely fulfilled without a greater understanding of enteric microbiota and its impact on mammalian physiology. By leveraging the knowledge gained through these studies, we will be prepared to enter the era of personalized medicine where clinical inventions can be custom-tailored to individual patients to achieve better outcomes.
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              Bacterial protein signals are associated with Crohn’s disease

              Objective No Crohn’s disease (CD) molecular maker has advanced to clinical use, and independent lines of evidence support a central role of the gut microbial community in CD. Here we explore the feasibility of extracting bacterial protein signals relevant to CD, by interrogating myriads of intestinal bacterial proteomes from a small number of patients and healthy controls. Design We first developed and validated a workflow—including extraction of microbial communities, two-dimensional difference gel electrophoresis (2D-DIGE), and LC-MS/MS—to discover protein signals from CD-associated gut microbial communities. Then we used selected reaction monitoring (SRM) to confirm a set of candidates. In parallel, we used 16S rRNA gene sequencing for an integrated analysis of gut ecosystem structure and functions. Results Our 2D-DIGE-based discovery approach revealed an imbalance of intestinal bacterial functions in CD. Many proteins, largely derived from Bacteroides species, were over-represented, while under-represented proteins were mostly from Firmicutes and some Prevotella members. Most overabundant proteins could be confirmed using SRM. They correspond to functions allowing opportunistic pathogens to colonise the mucus layers, breach the host barriers and invade the mucosae, which could still be aggravated by decreased host-derived pancreatic zymogen granule membrane protein GP2 in CD patients. Moreover, although the abundance of most protein groups reflected that of related bacterial populations, we found a specific independent regulation of bacteria-derived cell envelope proteins. Conclusions This study provides the first evidence that quantifiable bacterial protein signals are associated with CD, which can have a profound impact on future molecular diagnosis.
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                Author and article information

                Contributors
                Journal
                Genes Dis
                Genes Dis
                Genes & Diseases
                Chongqing Medical University
                2352-4820
                2352-3042
                18 October 2014
                December 2014
                18 October 2014
                : 1
                : 2
                : 130-131
                Affiliations
                [1]Department of Biochemistry, Rush University, Cohn Research Building, 1735 W. Harrison St., Chicago, IL 60612, USA
                Author notes
                []Tel: +1 (312) 942 5755; fax: +1 (312) 942 3053. jun_sun@ 123456rush.edu
                Article
                S2352-3042(14)00032-4
                10.1016/j.gendis.2014.09.008
                6146158
                cf22936f-624e-49f5-b1bf-257c32ba786b
                Copyright © 2014, Chongqing Medical University. Production and hosting by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

                History
                : 29 September 2014
                : 29 September 2014
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