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      The effects of probiotic and synbiotic supplementation on metabolic syndrome indices in adults at risk of type 2 diabetes: study protocol for a randomized controlled trial

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          Abstract

          Background

          The incidence of type 2 diabetes, cardiovascular diseases, and obesity has been rising dramatically; however, their pathogenesis is particularly intriguing. Recently, dysbiosis of the intestinal microbiota has emerged as a new candidate that may be linked to metabolic diseases. We hypothesize that selective modulation of the intestinal microbiota by probiotic or synbiotic supplementation may improve metabolic dysfunction and prevent diabetes in prediabetics. In this study, a synthesis and study of synbiotics will be carried out for the first time in Iran.

          Methods/Design

          In a randomized triple-blind controlled clinical trial, 120 adults with impaired glucose tolerance based on the inclusion criteria will be selected by a simple random sampling method and will be randomly allocated to 6 months of 6 g/d probiotic, synbiotic or placebo. The fecal abundance of bacteria, blood pressure, height, weight, and waist and hip circumferences will be measured at baseline and following treatment. Also, plasma lipid profiles, HbA1C, fasting plasma glucose, and insulin levels, will be measured and insulin resistance (HOMA-IR) and beta-cell function (HOMA-B) will be calculated at baseline and will be repeated at months 3, 6, 12, and 18. The data will be compared within and between groups using statistical methods.

          Discussion

          The results of this trial could contribute to the evidence-based clinical guidelines that address gut microbiota manipulation to maximize health benefits in prevention and management of metabolic syndrome in prediabetes.

          Trial registration

          Iranian Registry of Clinical Trials: IRCT201511032321N2. Registered on 27 February 2016.

          Electronic supplementary material

          The online version of this article (doi:10.1186/s13063-017-1885-8) contains supplementary material, which is available to authorized users.

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          Most cited references12

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          Compendium of physical activities: an update of activity codes and MET intensities.

          We provide an updated version of the Compendium of Physical Activities, a coding scheme that classifies specific physical activity (PA) by rate of energy expenditure. It was developed to enhance the comparability of results across studies using self-reports of PA. The Compendium coding scheme links a five-digit code that describes physical activities by major headings (e.g., occupation, transportation, etc.) and specific activities within each major heading with its intensity, defined as the ratio of work metabolic rate to a standard resting metabolic rate (MET). Energy expenditure in MET-minutes, MET-hours, kcal, or kcal per kilogram body weight can be estimated for specific activities by type or MET intensity. Additions to the Compendium were obtained from studies describing daily PA patterns of adults and studies measuring the energy cost of specific physical activities in field settings. The updated version includes two new major headings of volunteer and religious activities, extends the number of specific activities from 477 to 605, and provides updated MET intensity levels for selected activities.
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            Endotoxemia Is Associated With an Increased Risk of Incident Diabetes

            OBJECTIVE Diabetes is accompanied with a chronic low-grade inflammation, which may in part be mediated by endotoxins derived from Gram-negative bacteria. RESEARCH DESIGN AND METHODS We investigated in a population-based cohort whether endotoxemia is associated with clinically incident diabetes. The serum endotoxin activity was measured by limulus assay from the FINRISK97 cohort comprising 7,169 subjects aged 25–74 years and followed up for 10 years. RESULTS Both the subjects with prevalent diabetes (n = 537) and those with incident diabetes (n = 462) had higher endotoxin activity than the nondiabetic individuals (P < 0.001). The endotoxin activity was significantly associated with increased risk for incident diabetes with a hazard ratio 1.004 (95% CI 1.001–1.007; P = 0.019) per unit increase resulting in a 52% increased risk (P = 0.013) in the highest quartile compared with the lowest one. The association was independent of diabetes risk factors: serum lipids, γ-glutamyl transferase, C-reactive protein, BMI, and blood glucose. Furthermore, the association of endotoxemia with an increased risk of incident diabetes was independent of the metabolic syndrome as defined either by the National Cholesterol Educational Program-Adult Treatment Panel III or the International Diabetes Federation. Endotoxin activity was linearly related (P < 0.001) to the number of components of the metabolic syndrome. CONCLUSIONS Both prevalent and incident diabetes were associated with endotoxemia, which may link metabolic disorders to inflammation. The results suggest that microbes play a role in the pathogenesis of diabetes.
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              A microbial world within us.

              The microbial world within us includes a vast array of gastrointestinal (GI) tract communities that play an important role in health and disease. Significant progress has been made in recent years in describing the intestinal microbial composition based on the application of 16S ribosomal RNA (rRNA)-based approaches. These were not only instrumental in providing a phylogenetic framework of the more than 1000 different intestinal species but also illustrated the temporal and spatial diversity of the microbial GI tract composition that is host-specific and affected by the genotype. However, our knowledge of the molecular and cellular bases of host-microbe interactions in the GI tract is still very limited. Here an overview is presented of the most recent developments and applications of novel culture-independent approaches that promise to unravel the mechanisms of GI tract functionality and subsequent possibilities to exploit specifically these mechanisms in order to improve gut health.
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                Author and article information

                Contributors
                kasaeian@idrc.mui.ac.ir
                aminorroaya@med.mui.ac.ir
                00983133359359 , awat_feiz@hlth.mui.ac.ir
                p-jafari@iau-arak.ac.ir
                m_amini@med.mui.ac.ir
                Journal
                Trials
                Trials
                Trials
                BioMed Central (London )
                1745-6215
                29 March 2017
                29 March 2017
                2017
                : 18
                : 148
                Affiliations
                [1 ]ISNI 0000 0001 1498 685X, GRID grid.411036.1, Isfahan Endocrine and Metabolism Research Center, , Isfahan University of Medical Sciences, ; Isfahan, Iran
                [2 ]ISNI 0000 0001 1498 685X, GRID grid.411036.1, Biostatistics and Epidemiology Department, , School of Health, Cardiac Rehabilitation Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, ; Isfahan, Iran
                [3 ]ISNI 0000 0001 0706 2472, GRID grid.411463.5, Microbiology Departments, Science Faculty, , Islamic Azad University (IAU), ; Arak Branch, Arak, Iran
                Author information
                http://orcid.org/0000-0002-9724-2983
                Article
                1885
                10.1186/s13063-017-1885-8
                5372291
                28356129
                560d082d-cf6a-41ce-a13e-8fae53aafda0
                © The Author(s). 2017

                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. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 6 December 2016
                : 8 March 2017
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100003970, Isfahan University of Medical Sciences;
                Award ID: 394813
                Award Recipient :
                Categories
                Study Protocol
                Custom metadata
                © The Author(s) 2017

                Medicine
                probiotic,synbiotic,impaired glucose tolerance,metabolic syndrome,microbiome
                Medicine
                probiotic, synbiotic, impaired glucose tolerance, metabolic syndrome, microbiome

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