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      16S gut community of the Cameron County Hispanic Cohort

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          Abstract

          Background

          Obesity and type 2 diabetes (T2D) are major public health concerns worldwide, and their prevalence has only increased in recent years. Mexican Americans are disproportionately afflicted by obesity and T2D, and rates are even higher in the United States-Mexico border region. To determine the factors associated with the increased risk of T2D, obesity, and other diseases in this population, the Cameron County Hispanic Cohort was established in 2004.

          Results

          In this study, we characterized the 16S gut community of a subset of 63 subjects from this unique cohort. We found that these communities, when compared to Human Microbiome Project subjects, exhibit community shifts often observed in obese and T2D individuals in published studies. We also examined microbial network relationships between operational taxonomic units (OTUs) in the Cameron County Hispanic Cohort (CCHC) and three additional datasets. We identified a group of seven genera that form a tightly interconnected network present in all four tested datasets, dominated by butyrate producers, which are often increased in obese individuals while being depleted in T2D patients.

          Conclusions

          Through a combination of increased disease prevalence and relatively high gut microbial homogeneity in the subset of CCHC members we examined, we believe that the CCHC may represent an ideal community to dissect mechanisms underlying the role of the gut microbiome in human health and disease. The lack of CCHC subject gut community segregation based on all tested metadata suggests that the community structure we observe in the CCHC likely occurs early in life, and endures. This persistent ‘disease’-related gut microbial community in CCHC subjects may enhance existing genetic or lifestyle predispositions to the prevalent diseases of the CCHC, leading to increased attack rates of obesity, T2D, non-alcoholic fatty liver disease, and others.

          Electronic supplementary material

          The online version of this article (doi:10.1186/s40168-015-0072-y) contains supplementary material, which is available to authorized users.

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          Most cited references37

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          Fecal microbiome and volatile organic compound metabolome in obese humans with nonalcoholic fatty liver disease.

          The histopathology of nonalcoholic fatty liver disease (NAFLD) is similar to that of alcoholic liver disease. Colonic bacteria are a source of many metabolic products, including ethanol and other volatile organic compounds (VOC) that may have toxic effects on the human host after intestinal absorption and delivery to the liver via the portal vein. Recent data suggest that the composition of the gut microbiota in obese human beings is different from that of healthy-weight individuals. The aim of this study was to compare the colonic microbiome and VOC metabolome of obese NAFLD patients (n = 30) with healthy controls (n = 30). Multitag pyrosequencing was used to characterize the fecal microbiota. Fecal VOC profiles were measured by gas chromatography-mass spectrometry. There were statistically significant differences in liver biochemistry and metabolic parameters in NAFLD. Deep sequencing of the fecal microbiome revealed over-representation of Lactobacillus species and selected members of phylum Firmicutes (Lachnospiraceae; genera, Dorea, Robinsoniella, and Roseburia) in NAFLD patients, which was statistically significant. One member of phylum Firmicutes was under-represented significantly in the fecal microbiome of NAFLD patients (Ruminococcaceae; genus, Oscillibacter). Fecal VOC profiles of the 2 patient groups were different, with a significant increase in fecal ester compounds observed in NAFLD patients. A significant increase in fecal ester VOC is associated with compositional shifts in the microbiome of obese NAFLD patients. These novel bacterial metabolomic and metagenomic factors are implicated in the etiology and complications of obesity. Copyright © 2013 AGA Institute. Published by Elsevier Inc. All rights reserved.
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            Prevalence of diabetes and impaired fasting glucose in adults in the U.S. population: National Health And Nutrition Examination Survey 1999-2002.

            The purpose of this study was to examine the prevalences of diagnosed and undiagnosed diabetes, and impaired fasting glucose (IFG) in U.S. adults during 1999-2002, and compare prevalences to those in 1988-1994. The National Health and Nutrition Examination Survey (NHANES) contains a probability sample of adults aged > or =20 years. In the NHANES 1999-2002, 4,761 adults were classified on glycemic status using standard criteria, based on an interview for diagnosed diabetes and fasting plasma glucose measured in a subsample. The crude prevalence of total diabetes in 1999-2002 was 9.3% (19.3 million, 2002 U.S. population), consisting of 6.5% diagnosed and 2.8% undiagnosed. An additional 26.0% had IFG, totaling 35.3% (73.3 million) with either diabetes or IFG. The prevalence of total diabetes rose with age, reaching 21.6% for those aged > or =65 years. The prevalence of diagnosed diabetes was twice as high in non-Hispanic blacks and Mexican Americans compared with non-Hispanic whites (both P < 0.00001), whereas the prevalence of undiagnosed diabetes was similar by race/ethnicity, adjusted for age and sex. The prevalence of diagnosed diabetes was similar by sex, but prevalences of undiagnosed diabetes and IFG were significantly higher in men. The crude prevalence of diagnosed diabetes rose significantly from 5.1% in 1988-1994 to 6.5% in 1999-2002, but the crude prevalences were stable for undiagnosed diabetes (from 2.7 to 2.8%) and IFG (from 24.7 to 26.0%). Results were similar after adjustment for age and sex. Although the prevalence of diagnosed diabetes has increased significantly over the last decade, the prevalences of undiagnosed diabetes and IFG have remained relatively stable. Minority groups remain disproportionately affected.
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              Adiposity, gut microbiota and faecal short chain fatty acids are linked in adult humans

              Background/Objectives: High dietary fibre intakes may protect against obesity by influencing colonic fermentation and the colonic microbiota. Though, recent studies suggest that increased colonic fermentation contributes to adiposity. Diet influences the composition of the gut microbiota. Previous research has not evaluated dietary intakes, body mass index (BMI), faecal microbiota and short chain fatty acid (SCFA) in the same cohort. Our objectives were to compare dietary intakes, faecal SCFA concentrations and gut microbial profiles in healthy lean (LN, BMI⩽25) and overweight or obese (OWOB, BMI>25) participants. Design: We collected demographic information, 3-day diet records, physical activity questionnaires and breath and faecal samples from 94 participants of whom 52 were LN and 42 OWOB. Results: Dietary intakes and physical activity levels did not differ significantly between groups. OWOB participants had higher faecal acetate (P=0.05), propionate (P=0.03), butyrate (P=0.05), valerate (P=0.03) and total short chain fatty acid (SCFA; P=0.02) concentrations than LN. No significant differences in Firmicutes to Bacteroides/Prevotella (F:B) ratio was observed between groups. However, in the entire cohort, Bacteroides/Prevotella counts were negatively correlated with faecal total SCFA (r=−0.32, P=0.002) and F:B ratio was positively correlated with faecal total SCFA (r=0.42, P<0.0001). Principal component analysis identified distinct gut microbiota and SCFA–F:B ratio components, which together accounted for 59% of the variation. F:B ratio loaded with the SCFA and not with the microbiota suggesting that SCFA and F:B ratio vary together and may be interrelated. Conclusions: The results support the hypothesis that colonic fermentation patterns may be altered, leading to different faecal SCFA concentrations in OWOB compared with LN humans. More in-depth studies looking at the metabolic fate of SCFA produced in LN and OWOB participants are needed in order to determine the role of SCFA in obesity.
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                Author and article information

                Contributors
                mcross@bcm.edu
                donnam@bcm.edu
                joseph.b.mccormick@uth.tmc.edu
                agibbs@bcm.edu
                Susan.P.Fisher-Hoch@uth.tmc.edu
                jpetrosi@bcm.edu
                Journal
                Microbiome
                Microbiome
                Microbiome
                BioMed Central (London )
                2049-2618
                6 March 2015
                6 March 2015
                2015
                : 3
                : 7
                Affiliations
                [ ]Alkek Center for Metagenomics and Microbiome Research, Baylor College of Medicine, Houston, TX USA
                [ ]Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX USA
                [ ]Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX USA
                [ ]University of Texas School of Public Health, Brownsville, TX USA
                Article
                72
                10.1186/s40168-015-0072-y
                4355967
                25763184
                96267b3b-254b-446f-a157-6ef4f3b7f03e
                © Ross et al.; licensee BioMed Central. 2015

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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
                : 21 October 2014
                : 3 February 2015
                Categories
                Research
                Custom metadata
                © The Author(s) 2015

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