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      The Therapeutic Potential of Resistant Starch in Modulation of Insulin Resistance, Endotoxemia, Oxidative Stress and Antioxidant Biomarkers in Women with Type 2 Diabetes: A Randomized Controlled Clinical Trial

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          Abstract

          Aims: This trial aims to determine the effects of resistant starch (RS) subtype 2 (RS2) on glycemic status, metabolic endotoxemia and markers of oxidative stress. Methods: A randomized, controlled, parallel-group clinical trial group of 56 females with type 2 diabetes mellitus (T2DM) was divided to 2 groups. The intervention group (n = 28) and control group (n = 28) received 10 g/day RS2 or placebo for 8 weeks, respectively. Fasting blood samples were taken to determine glycemic status, endotoxin, high sensitivity C-reactive protein (hs-CRP), malondialdehyde (MDA), total antioxidant capacity (TAC), antioxidant enzymes concentrations as well as uric acid at baseline and after the intervention. Results: After 8 weeks, RS2 caused a significant decrease in the levels of MDA (-34.10%), glycosylated hemoglobin (-9.40%), insulin (-29.36%), homeostasis model of insulin resistance (-32.85%) and endotoxin (-25.00%), a significant increase in TAC (18.10%) and glutathione peroxidase (11.60%) as compared with control. No significant changes were observed in fasting plasma glucose, quantitative insulin sensitivity check index, hs-CRP, superoxide dismutase, catalase and uric acid in the RS2 group as compared with the control group. Conclusion: Supplementation with RS2 may be improved glycemic status, endotoxemia and markers of oxidative stress in patients with T2DM.

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          Butyrate inhibits inflammatory responses through NFkappaB inhibition: implications for Crohn's disease.

          J.-P. Segain (2000)
          Proinflammatory cytokines are key factors in the pathogenesis of Crohn's disease (CD). Activation of nuclear factor kappa B (NFkappaB), which is involved in their gene transcription, is increased in the intestinal mucosa of CD patients. As butyrate enemas may be beneficial in treating colonic inflammation, we investigated if butyrate promotes this effect by acting on proinflammatory cytokine expression. Intestinal biopsy specimens, isolated lamina propria cells (LPMC), and peripheral blood mononuclear cells (PBMC) were cultured with or without butyrate for assessment of secretion of tumour necrosis factor (TNF) and mRNA levels. NFkappaB p65 activation was determined by immunofluorescence and gene reporter experiments. Levels of NFkappaB inhibitory protein (IkappaBalpha) were analysed by western blotting. The in vivo efficacy of butyrate was assessed in rats with trinitrobenzene sulphonic acid (TNBS) induced colitis. Butyrate decreased TNF production and proinflammatory cytokine mRNA expression by intestinal biopsies and LPMC from CD patients. Butyrate abolished lipopolysaccharide (LPS) induced expression of cytokines by PBMC and transmigration of NFkappaB from the cytoplasm to the nucleus. LPS induced NFkappaB transcriptional activity was decreased by butyrate while IkappaBalpha levels were stable. Butyrate treatment also improved TNBS induced colitis. Butyrate decreases proinflammatory cytokine expression via inhibition of NFkappaB activation and IkappaBalpha degradation. These anti-inflammatory properties provide a rationale for assessing butyrate in the treatment of CD.
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            Diabetes, obesity and gut microbiota.

            Amandine Everard, Patrice Cani (2013)
            The gut microbiota composition has been associated with several hallmarks of metabolic syndrome (e.g., obesity, type 2 diabetes, cardiovascular diseases, and non-alcoholic steatohepatitis). Growing evidence suggests that gut microbes contribute to the onset of the low-grade inflammation characterising these metabolic disorders via mechanisms associated with gut barrier dysfunctions. Recently, enteroendocrine cells and the endocannabinoid system have been shown to control gut permeability and metabolic endotoxaemia. Moreover, targeted nutritional interventions using non-digestible carbohydrates with prebiotic properties have shown promising results in pre-clinical studies in this context, although human intervention studies warrant further investigations. Thus, in this review, we discuss putative mechanisms linking gut microbiota and type 2 diabetes. These data underline the advantage of investigating and changing the gut microbiota as a therapeutic target in the context of obesity and type 2 diabetes. Copyright © 2013 Elsevier Ltd. All rights reserved.
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              Resistant starch improves insulin sensitivity in metabolic syndrome.

              Chris Thomas, G Frost, Linda J. Bell … (2010)
              Diets rich in non-viscous fibre are linked to a reduced risk of both diabetes and cardiovascular disease; however, the mechanism of action remains unclear. This study was undertaken to assess whether chronic consumption of this type of fibre in individuals with the metabolic syndrome would improve insulin sensitivity via changes in ectopic fat storage. The study was a single-blind, randomized, parallel nutritional intervention where 20 insulin resistant subjects consumed either the fibre supplement (resistant starch) (40 g/day) or placebo supplement (0 g/day) for 12 weeks. Insulin sensitivity was measured by euglycaemic-hyperinsulinaemic clamp and ectopic fat storage measured by whole-body magnetic resonance spectroscopy. Resistant starch consumption did not significantly affect body weight, fat storage in muscle, liver or visceral depots. There was also no change with resistant starch feeding on vascular function or markers of inflammation. However, in subjects randomized to consume the resistant starch, insulin sensitivity improved compared with the placebo group (P = 0.023). Insulin sensitivity correlated significantly with changes in waist circumference and fat storage in tibialis muscle and to a lesser extent to visceral-to-subcutaneous abdominal adipose tissue ratio. Consumption of resistant starch improves insulin sensitivity in subjects with the metabolic syndrome. Unlike in animal models, diabetes prevention does not appear to be directly related to changes in body adiposity, blood lipids or inflammatory markers. Further research to elucidate the mechanisms behind this change in insulin sensitivity in human subjects is required.
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                Author and article information

                Journal
                Journal ID (publisher-id): ANM
                Journal ID (nlm-ta): Ann Nutr Metab
                Journal ID (doi): 10.1159/issn.0250-6807
                Title: Annals of Nutrition and Metabolism
                Abbreviated Title: Ann Nutr Metab
                Publisher: S. Karger AG (Basel, Switzerland karger@ 123456karger.com http://www.karger.com )
                ISSN (Print): 0250-6807
                ISSN (Electronic): 1421-9697
                Publication date (Print): February 2016
                Publication date (Electronic): 12 December 2015
                Volume: 68
                Issue: 2
                Pages: 85-93
                Affiliations
                aNeurosciences Research Center, bDepartment of Community Nutrition, Faculty of Nutrition, cDepartment of Biochemistry and Nutrition, Faculty of Nutrition, dDepartment of Emergency Medicine, and eNutrition Research Center, Department Food Science and Technology, Faculty of Nutrition, Tabriz University of Medical Sciences, Tabriz, and fNutrition and Metabolic Diseases Research Center, Hyperlipidemia Research Center, Ahvaz Jundishapur, University of Medical Sciences, Ahwaz, Iran; gDepartment of Nutrition and Dietetics, Faculty of Medicine and Health Sciences, University Putra Malaysia, Selangor, Malaysia
                Article
                Publisher ID: ANM2016068002085 Other ID: Ann Nutr Metab 2016;68:85-93
                DOI: 10.1159/000441683
                PubMed ID: 26655398
                SO-VID: 41aa6387-3e5d-45e9-91ee-546b78931ce2
                Copyright © © 2015 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 29 March 2015
                Date accepted : 11 October 2015
                Page count
                Figures: 1, Tables: 4, References: 37, Pages: 9
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Medicine,General social science
                Keywords: Type 2 diabetes,Insulin,Endotoxemia,Malondialdehde,Antioxidant,Resistant starch
                Data availability:
                ScienceOpen disciplines: Medicine, General social science
                Keywords: Type 2 diabetes, Insulin, Endotoxemia, Malondialdehde, Antioxidant, Resistant starch

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