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      Glucose- and glycaemic factor-lowering effects of probiotics on diabetes: a meta-analysis of randomised placebo-controlled trials

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      British Journal of Nutrition
      Cambridge University Press (CUP)

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          Abstract

          This meta-analysis examined the effect of probiotics on glucose and glycaemic factors in diabetes and its associated risk factors. All randomised-controlled trials published in English in multiple databases from January 2000 to June 2015 were systematically searched. Only studies that addressed glucose- and glycaemic-related factors as outcome variables were included. The main outcomes of interest in trials were mean changes in glucose, HbA1c, insulin and homoeostasis model assessment-estimated insulin resistance (HOMA-IR). Using the Physiotherapy Evidence Database (PEDro) scale to assess the quality of studies, a total of eleven studies with 614 subjects were included. The pooled mean difference and effect size with a 95 % CI were extracted using a random-effect model. It was found that there are statistically significant pooled mean differences between the probiotics and the placebo-controlled groups on the reduction of glucose (−0·52 mmol/l, 95 % CI −0·92, −0·11 mmol/l; P=0·01) and HbA1c (−0·32 %, 95 % CI −0·57, −0·07 %; P=0·01). There was no statistically significant pooled mean difference between the probiotics and the placebo-controlled groups on the reduction of insulin (−0·48 µIU/ml, 95 % CI −1·34, 0·38 µIU/ml; P=0·27) and HOMA-IR (pooled effect of –0·44, 95 % CI −1·57, 0·70; P=0·45). Meta-regression analysis identified that probiotics had significant effects on reduction of glucose, HbA1c, insulin and HOMA-IR in participants with diabetes, but not in participants with other risk factors. The present meta-analysis suggested that probiotics may be used as an important dietary supplement in reducing the glucose metabolic factors associated with diabetes.

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          Bias in meta-analysis detected by a simple, graphical test

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            Gut Microbiota in Human Adults with Type 2 Diabetes Differs from Non-Diabetic Adults

            Background Recent evidence suggests that there is a link between metabolic diseases and bacterial populations in the gut. The aim of this study was to assess the differences between the composition of the intestinal microbiota in humans with type 2 diabetes and non-diabetic persons as control. Methods and Findings The study included 36 male adults with a broad range of age and body-mass indices (BMIs), among which 18 subjects were diagnosed with diabetes type 2. The fecal bacterial composition was investigated by real-time quantitative PCR (qPCR) and in a subgroup of subjects (N = 20) by tag-encoded amplicon pyrosequencing of the V4 region of the 16S rRNA gene. The proportions of phylum Firmicutes and class Clostridia were significantly reduced in the diabetic group compared to the control group (P = 0.03). Furthermore, the ratios of Bacteroidetes to Firmicutes as well as the ratios of Bacteroides-Prevotella group to C. coccoides-E. rectale group correlated positively and significantly with plasma glucose concentration (P = 0.04) but not with BMIs. Similarly, class Betaproteobacteria was highly enriched in diabetic compared to non-diabetic persons (P = 0.02) and positively correlated with plasma glucose (P = 0.04). Conclusions The results of this study indicate that type 2 diabetes in humans is associated with compositional changes in intestinal microbiota. The level of glucose tolerance should be considered when linking microbiota with metabolic diseases such as obesity and developing strategies to control metabolic diseases by modifying the gut microbiota.
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              Colonic health: fermentation and short chain fatty acids.

              Interest has been recently rekindled in short chain fatty acids (SCFAs) with the emergence of prebiotics and probiotics aimed at improving colonic and systemic health. Dietary carbohydrates, specifically resistant starches and dietary fiber, are substrates for fermentation that produce SCFAs, primarily acetate, propionate, and butyrate, as end products. The rate and amount of SCFA production depends on the species and amounts of microflora present in the colon, the substrate source and gut transit time. SCFAs are readily absorbed. Butyrate is the major energy source for colonocytes. Propionate is largely taken up by the liver. Acetate enters the peripheral circulation to be metabolized by peripheral tissues. Specific SCFA may reduce the risk of developing gastrointestinal disorders, cancer, and cardiovascular disease. Acetate is the principal SCFA in the colon, and after absorption it has been shown to increase cholesterol synthesis. However, propionate, a gluconeogenerator, has been shown to inhibit cholesterol synthesis. Therefore, substrates that can decrease the acetate: propionate ratio may reduce serum lipids and possibly cardiovascular disease risk. Butyrate has been studied for its role in nourishing the colonic mucosa and in the prevention of cancer of the colon, by promoting cell differentiation, cell-cycle arrest and apoptosis of transformed colonocytes; inhibiting the enzyme histone deacetylase and decreasing the transformation of primary to secondary bile acids as a result of colonic acidification. Therefore, a greater increase in SCFA production and potentially a greater delivery of SCFA, specifically butyrate, to the distal colon may result in a protective effect. Butyrate irrigation (enema) has also been suggested in the treatment of colitis. More human studies are now needed, especially, given the diverse nature of carbohydrate substrates and the SCFA patterns resulting from their fermentation. Short-term and long-term human studies are particularly required on SCFAs in relation to markers of cancer risk. These studies will be key to the success of dietary recommendations to maximize colonic disease prevention.
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                Author and article information

                Journal
                British Journal of Nutrition
                Br J Nutr
                Cambridge University Press (CUP)
                0007-1145
                1475-2662
                April 14 2016
                February 22 2016
                April 14 2016
                : 115
                : 7
                : 1167-1177
                Article
                10.1017/S0007114516000076
                26899960
                41bba684-fc5b-40d8-abb8-b11240171a6f
                © 2016

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