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      Oral administration of Bifidobacterium breve B-3 modifies metabolic functions in adults with obese tendencies in a randomised controlled trial

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          Abstract

          Accumulating evidence suggests an association between gut microbiota and the development of obesity, raising the possibility of probiotic administration as a therapeutic approach. Bifidobacterium breve B-3 was found to exhibit an anti-obesity effect on high-fat diet-induced obesity mice. In the present study, a randomised, double-blind, placebo-controlled trial was conducted to evaluate the effect of the consumption of B. breve B-3 on body compositions and blood parameters in adults with a tendency for obesity. After a 4-week run-in period, the participants were randomised to receive either placebo or a B-3 capsule (approximately 5 × 10 10 colony-forming units of B-3/d) daily for 12 weeks. A significantly lowered fat mass was observed in the B-3 group compared with the placebo group at week 12. Improvements were observed for some blood parameters related to liver functions and inflammation, such as γ-glutamyltranspeptidase and high-sensitivity C-reactive protein. Significant correlations were found between the changed values of some blood parameters and the changed fat mass in the B-3 group. These results suggest the beneficial potential of B. breve B-3 in improving metabolic disorders.

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          Most cited references 29

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          Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Framingham Heart Study.

          Visceral adipose tissue (VAT) compartments may confer increased metabolic risk. The incremental utility of measuring both visceral and subcutaneous abdominal adipose tissue (SAT) in association with metabolic risk factors and underlying heritability has not been well described in a population-based setting. Participants (n=3001) were drawn from the Framingham Heart Study (48% women; mean age, 50 years), were free of clinical cardiovascular disease, and underwent multidetector computed tomography assessment of SAT and VAT volumes between 2002 and 2005. Metabolic risk factors were examined in relation to increments of SAT and VAT after multivariable adjustment. Heritability was calculated using variance-components analysis. Among both women and men, SAT and VAT were significantly associated with blood pressure, fasting plasma glucose, triglycerides, and high-density lipoprotein cholesterol and with increased odds of hypertension, impaired fasting glucose, diabetes mellitus, and metabolic syndrome (P range < 0.01). In women, relations between VAT and risk factors were consistently stronger than in men. However, VAT was more strongly correlated with most metabolic risk factors than was SAT. For example, among women and men, both SAT and VAT were associated with increased odds of metabolic syndrome. In women, the odds ratio (OR) of metabolic syndrome per 1-standard deviation increase in VAT (OR, 4.7) was stronger than that for SAT (OR, 3.0; P for difference between SAT and VAT < 0.0001); similar differences were noted for men (OR for VAT, 4.2; OR for SAT, 2.5). Furthermore, VAT but not SAT contributed significantly to risk factor variation after adjustment for body mass index and waist circumference (P < or = 0.01). Among overweight and obese individuals, the prevalence of hypertension, impaired fasting glucose, and metabolic syndrome increased linearly and significantly across increasing VAT quartiles. Heritability values for SAT and VAT were 57% and 36%, respectively. Although both SAT and VAT are correlated with metabolic risk factors, VAT remains more strongly associated with an adverse metabolic risk profile even after accounting for standard anthropometric indexes. Our findings are consistent with the hypothesized role of visceral fat as a unique, pathogenic fat depot. Measurement of VAT may provide a more complete understanding of metabolic risk associated with variation in fat distribution.
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            Obesity

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              Insulin sensitivity: modulation by nutrients and inflammation.

              Insulin resistance is a major metabolic feature of obesity and is a key factor in the etiology of a number of diseases, including type 2 diabetes. In this review, we discuss potential mechanisms by which brief nutrient excess and obesity lead to insulin resistance and propose that these mechanisms of action are different but interrelated. We discuss how pathways that "sense" nutrients within skeletal muscle are readily able to regulate insulin action. We then discuss how obesity leads to insulin resistance via a complex interplay among systemic fatty acid excess, microhypoxia in adipose tissue, ER stress, and inflammation. In particular, we focus on the hypothesis that the macrophage is an important cell type in the propagation of inflammation and induction of insulin resistance in obesity. Overall, we provide our integrative perspective regarding how nutrients and obesity interact to regulate insulin sensitivity.
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                Author and article information

                Journal
                J Nutr Sci
                J Nutr Sci
                JNS
                Journal of Nutritional Science
                Cambridge University Press (Cambridge, UK )
                2048-6790
                2015
                4 May 2015
                : 4
                Affiliations
                [1 ]Food Science and Technology Institute , Morinaga Milk Industry Co. Ltd, Zama, Kanagawa, Japan
                [2 ]Nutritional Science Institute , Morinaga Milk Industry Co. Ltd, Zama, Kanagawa, Japan
                [3 ]NAKAJIMA Medical Clinic , Yokosuka, Kanagawa, Japan
                [4 ]Division of Healthcare Graduate School, Tokyo Healthcare University , Setagaya, Tokyo, Japan
                Author notes
                [* ]Corresponding author:, Dr Jun-ichi Minami, email j-minami@ 123456morinagamilk.co.jp
                Article
                S2048679015000051 00005
                10.1017/jns.2015.5
                4463018
                © The Author(s) 2015

                This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence ( http://creativecommons.org/licenses/by/3.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Page count
                Figures: 2, Tables: 3, References: 46, Pages: 25
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