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      Soy Improves Cardiometabolic Health and Cecal Microbiota in Female Low-Fit Rats

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          Abstract

          Phytoestrogen-rich soy is known to ameliorate menopause-associated obesity and metabolic dysfunction for reasons that are unclear. The gut microbiota have been linked with the development of obesity and metabolic dysfunction. We aimed to determine the impact of soy on cardiometabolic health, adipose tissue inflammation, and the cecal microbiota in ovariectomized (OVX) rats bred for low-running capacity (LCR), a model that has been previously shown to mimic human menopause compared to sham-operated (SHM) intact control LCR rats. In this study, soy consumption, without affecting energy intake or physical activity, significantly improved insulin sensitivity and body composition of OVX rats bred for low-running capacity. Furthermore, soy significantly improved blood lipid profile, adipose tissue inflammation, and aortic stiffness of LCR rats. Compared to a soy-free control diet, soy significantly shifted the cecal microbial community of LCR rats, resulting in a lower Firmicutes:Bacteroidetes ratio. Correlations among metabolic parameters and cecal bacterial taxa identified in this study suggest that taxa Prevotella, Dorea, and Phascolarctobacterium may be taxa of interest. Our results suggest that dietary soy ameliorates adiposity, insulin sensitivity, adipose tissue inflammation, and arterial stiffness and exerts a beneficial shift in gut microbial communities in a rat model that mimics human menopause.

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          Adipocyte death, adipose tissue remodeling, and obesity complications.

          We sought to determine the role of adipocyte death in obesity-induced adipose tissue (AT) inflammation and obesity complications. Male C57BL/6 mice were fed a high-fat diet for 20 weeks to induce obesity. Every 4 weeks, insulin resistance was assessed by intraperitoneal insulin tolerance tests, and epididymal (eAT) and inguinal subcutaneous AT (iAT) and livers were harvested for histological, immunohistochemical, and gene expression analyses. Frequency of adipocyte death in eAT increased from <0.1% at baseline to 16% at week 12, coincident with increases in 1) depot weight; 2) AT macrophages (ATM Phi s) expressing F4/80 and CD11c; 3) mRNA for tumor necrosis factor (TNF)-alpha, monocyte chemotactic protein (MCP)-1, and interleukin (IL)-10; and 4) insulin resistance. ATM Phi s in crown-like structures surrounding dead adipocytes expressed TNF-alpha and IL-6 proteins. Adipocyte number began to decline at week 12. At week 16, adipocyte death reached approximately 80%, coincident with maximal expression of CD11c and inflammatory genes, loss (40%) of eAT mass, widespread collagen deposition, and accelerated hepatic macrosteatosis. By week 20, adipocyte number was restored with small adipocytes, coincident with reduced adipocyte death (fourfold), CD11c and MCP-1 gene expression (twofold), and insulin resistance (35%). eAT weight did not increase at week 20 and was inversely correlated with liver weight after week 12 (r = -0. 85, P < 0.001). In iAT, adipocyte death was first detected at week 12 and remained
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            The pros and cons of phytoestrogens.

            Phytoestrogens are plant derived compounds found in a wide variety of foods, most notably soy. A litany of health benefits including a lowered risk of osteoporosis, heart disease, breast cancer, and menopausal symptoms, are frequently attributed to phytoestrogens but many are also considered endocrine disruptors, indicating that they have the potential to cause adverse health effects as well. Consequently, the question of whether or not phytoestrogens are beneficial or harmful to human health remains unresolved. The answer is likely complex and may depend on age, health status, and even the presence or absence of specific gut microflora. Clarity on this issue is needed because global consumption is rapidly increasing. Phytoestrogens are present in numerous dietary supplements and widely marketed as a natural alternative to estrogen replacement therapy. Soy infant formula now constitutes up to a third of the US market, and soy protein is now added to many processed foods. As weak estrogen agonists/antagonists with molecular and cellular properties similar to synthetic endocrine disruptors such as Bisphenol A (BPA), the phytoestrogens provide a useful model to comprehensively investigate the biological impact of endocrine disruptors in general. This review weighs the evidence for and against the purported health benefits and adverse effects of phytoestrogens. Copyright © 2010. Published by Elsevier Inc.
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              Cardiovascular risk factors emerge after artificial selection for low aerobic capacity.

              In humans, the strong statistical association between fitness and survival suggests a link between impaired oxygen metabolism and disease. We hypothesized that artificial selection of rats based on low and high intrinsic exercise capacity would yield models that also contrast for disease risk. After 11 generations, rats with low aerobic capacity scored high on cardiovascular risk factors that constitute the metabolic syndrome. The decrease in aerobic capacity was associated with decreases in the amounts of transcription factors required for mitochondrial biogenesis and in the amounts of oxidative enzymes in skeletal muscle. Impairment of mitochondrial function may link reduced fitness to cardiovascular and metabolic disease.
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                Author and article information

                Contributors
                vieirapotterv@missouri.edu
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                23 August 2017
                23 August 2017
                2017
                : 7
                : 9261
                Affiliations
                [1 ]ISNI 0000 0004 1936 9991, GRID grid.35403.31, Division of Nutritional Sciences, , University of Illinois at Urbana-Champaign, ; Urbana, IL 61801 USA
                [2 ]ISNI 0000 0004 1936 9991, GRID grid.35403.31, Department of Animal Sciences, , University of Illinois at Urbana-Champaign, ; Urbana, IL 61801 USA
                [3 ]ISNI 0000 0001 2162 3504, GRID grid.134936.a, Department of Nutrition and Exercise Physiology, , University of Missouri, ; Columbia, MO 65211 USA
                [4 ]ISNI 0000 0001 2162 3504, GRID grid.134936.a, Department of Biomedical Sciences, , University of Missouri, ; Columbia, MO 65211 USA
                [5 ]ISNI 0000 0001 2162 3504, GRID grid.134936.a, Department of Child Health, , University of Missouri, ; Columbia, MO 65211 USA
                [6 ]ISNI 0000 0001 2162 3504, GRID grid.134936.a, Dalton Cardiovascular Research Center, , University of Missouri, ; Columbia, MO 65211 USA
                [7 ]ISNI 0000000086837370, GRID grid.214458.e, Department of Anesthesiology, , University of Michigan, ; Ann Arbor, MI 48109 USA
                [8 ]ISNI 0000000086837370, GRID grid.214458.e, Department of Molecular & Integrative Physiology, , University of Michigan, ; Ann Arbor, MI 48109 USA
                Author information
                http://orcid.org/0000-0002-8856-8578
                Article
                8965
                10.1038/s41598-017-08965-0
                5569109
                28835674
                ad823061-115d-4ec9-b444-9c22ff3d5000
                © The Author(s) 2017

                Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 23 January 2017
                : 20 July 2017
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