For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
6
views
47
references
 Top references
cited by
19
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      195
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      A randomised placebo controlled trial of VSL#3 ® probiotic on biomarkers of cardiovascular risk and liver injury in non-alcoholic fatty liver disease

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Non-alcoholic fatty liver disease (NAFLD) is associated with increased cardiovascular risk irrespective of conventional risk factors. The role of gut-liver interaction is implicated in its development. We investigated the effects of VSL#3 ® probiotic supplementation on biomarkers of cardiovascular risk and liver injury in patients with NAFLD.

          Methods

          A randomised, double-blinded, placebo-controlled, proof-of-concept study was undertaken. Patients with NAFLD were randomly allocated to take 2 sachets VSL#3 ® probiotic or placebo twice daily for 10 weeks. Measurements of endothelial function (digital photoplethysmography, sVCAM-1 and cGMP), oxidative stress (glutathione ratio and LHP), inflammation (hsCRP), insulin resistance (HOMA-IR) and liver injury [transaminases, fibrosis risk score and acoustic structure quantification (ASQ)] were undertaken before and after intervention. Difference in baseline characteristics between the treatment groups was analysed using independent t-test or Mann Whitney U test for non-parametric data. Independent t-test was used to compare the outcomes at the end of the study between the two treatment groups. Wilcoxon Signed Rank test was used to determine the difference in fibrosis risk scores before and after treatment. Spearman’s correlation was used to determine any association between cardiovascular and hepatic markers at baseline.

          Results

          Thirty-five patients completed the study (28 males and 7 females) with a mean age of 57 ± 8 years, body mass index of 32.6 ± 5.0 kg/m 2 and a relatively short duration of NAFLD (median duration 0.3 IQR 2.0 years). No significant difference was observed in biomarkers of cardiovascular risk and liver injury following VSL#3 ® supplementation. Significant correlations were noted between sVCAM-1 and hsCRP (rho = 0.392, p = 0.01), and HOMA-IR and AST (rho = 0.489, p < 0.01) at baseline.

          Conclusions

          This is the first study to evaluate the effect of VSL#3 ® on ASQ in patients with NAFLD. VSL#3 ® did not significantly improve markers of cardiovascular risk and liver injury in patients with NAFLD. However, the study supports an association between endothelial dysfunction and inflammation in patients with NAFLD and suggests that NAFLD is linked with insulin resistance.

          Trial registration: ISRCTN05474560 ( https://doi.org/10.1186/ISRCTN05474560) Registered 9 August 2012 (retrospectively registered).

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12876-021-01660-5.

          Related collections

          Most cited references47

          • Record: found
          • Abstract: found
          • Article: not found

          Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

          D. Matthews, J Hosker, A Rudenski … (1985)
          The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
          Article 0 comments Cited 1737 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention

            Zobair Younossi, Quentin M Anstee, Milena Marietti … (2018)
            NAFLD is one of the most important causes of liver disease worldwide and will probably emerge as the leading cause of end-stage liver disease in the coming decades, with the disease affecting both adults and children. The epidemiology and demographic characteristics of NAFLD vary worldwide, usually parallel to the prevalence of obesity, but a substantial proportion of patients are lean. The large number of patients with NAFLD with potential for progressive liver disease creates challenges for screening, as the diagnosis of NASH necessitates invasive liver biopsy. Furthermore, individuals with NAFLD have a high frequency of metabolic comorbidities and could place a growing strain on health-care systems from their need for management. While awaiting the development effective therapies, this disease warrants the attention of primary care physicians, specialists and health policy makers.
            Article 0 comments Cited 1589 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Metabolic endotoxemia initiates obesity and insulin resistance.

              Patrice Cani, Jacques Amar, Miguel Angel Iglesias … (2007)
              Diabetes and obesity are two metabolic diseases characterized by insulin resistance and a low-grade inflammation. Seeking an inflammatory factor causative of the onset of insulin resistance, obesity, and diabetes, we have identified bacterial lipopolysaccharide (LPS) as a triggering factor. We found that normal endotoxemia increased or decreased during the fed or fasted state, respectively, on a nutritional basis and that a 4-week high-fat diet chronically increased plasma LPS concentration two to three times, a threshold that we have defined as metabolic endotoxemia. Importantly, a high-fat diet increased the proportion of an LPS-containing microbiota in the gut. When metabolic endotoxemia was induced for 4 weeks in mice through continuous subcutaneous infusion of LPS, fasted glycemia and insulinemia and whole-body, liver, and adipose tissue weight gain were increased to a similar extent as in high-fat-fed mice. In addition, adipose tissue F4/80-positive cells and markers of inflammation, and liver triglyceride content, were increased. Furthermore, liver, but not whole-body, insulin resistance was detected in LPS-infused mice. CD14 mutant mice resisted most of the LPS and high-fat diet-induced features of metabolic diseases. This new finding demonstrates that metabolic endotoxemia dysregulates the inflammatory tone and triggers body weight gain and diabetes. We conclude that the LPS/CD14 system sets the tone of insulin sensitivity and the onset of diabetes and obesity. Lowering plasma LPS concentration could be a potent strategy for the control of metabolic diseases.
              Article 0 comments Cited 1117 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Pui Lin Chong:
                ORCID: http://orcid.org/0000-0002-7747-4162
                linachong1@gmail.com
                Journal
                Journal ID (nlm-ta): BMC Gastroenterol
                Journal ID (iso-abbrev): BMC Gastroenterol
                Title: BMC Gastroenterology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1471-230X
                Publication date (Electronic): 1 April 2021
                Publication date PMC-release: 1 April 2021
                Publication date Collection: 2021
                Volume: 21
                Electronic Location Identifier: 144
                Affiliations
                [1 ]GRID grid.415470.3, ISNI 0000 0004 0392 0072, Academic Department of Diabetes and Endocrinology, , Queen Alexandra Hospital, ; Portsmouth, UK
                [2 ]GRID grid.4701.2, ISNI 0000 0001 0728 6636, School of Pharmacy and Biomedical Sciences, , University of Portsmouth, ; Portsmouth, UK
                [3 ]GRID grid.415470.3, ISNI 0000 0004 0392 0072, Department of Gastroenterology and Hepatology, , Queen Alexandra Hospital, ; Portsmouth, UK
                [4 ]GRID grid.415470.3, ISNI 0000 0004 0392 0072, Radiology Department, , Queen Alexandra Hospital, ; Portsmouth, UK
                [5 ]GRID grid.415631.4, ISNI 0000 0004 0600 1442, Raja Isteri Pengiran Anak Saleha Hospital, ; Bandar Seri Begawan, 1710 Brunei Darussalam
                Author information
                http://orcid.org/0000-0002-7747-4162
                Article
                Publisher ID: 1660
                DOI: 10.1186/s12876-021-01660-5
                PMC ID: 8015038
                PubMed ID: 33794784
                SO-VID: 5c49997b-e018-4e7f-8a87-388fa8371693
                Copyright © © The Author(s) 2021
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

                History
                Date received : 12 August 2019
                Date accepted : 9 February 2021
                Funding
                Funded by: Actial Farmaceutica, Italy
                Funded by: Portsmouth Hospitals NHS Trust
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2021

                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: fatty liver,probiotic,biomarkers
                Data availability:
                ScienceOpen disciplines: Gastroenterology & Hepatology
                Keywords: fatty liver, probiotic, biomarkers

                Comments

                Comment on this article

                scite_

                Similar content195

                See all similar

                Cited by19

                See all cited by

                Most referenced authors1,291

                See all reference authors