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      Green tea extracts ameliorate high-fat diet–induced muscle atrophy in senescence-accelerated mouse prone-8 mice

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          Abstract

          Muscle atrophy (loss of skeletal muscle mass) causes progressive deterioration of skeletal function. Recently, excessive intake of fats was suggested to induce insulin resistance, followed by muscle atrophy. Green tea extracts (GTEs), which contain polyphenols such as epigallocatechin gallate, have beneficial effects on obesity, hyperglycemia, and insulin resistance, but their effects against muscle atrophy are still unclear. Here, we found that GTEs prevented high-fat (HF) diet–induced muscle weight loss in senescence-accelerated mouse prone-8 (SAMP8), a murine model of senescence. SAMP8 mice were fed a control diet, an HF diet, or HF with 0.5% GTEs (HFGT) diet for 4 months. The HF diet induced muscle weight loss with aging (measured as quadriceps muscle weight), whereas GTEs prevented this loss. In HF diet–fed mice, blood glucose and plasma insulin concentrations increased in comparison with the control group, and these mice had insulin resistance as determined by homeostasis model assessment of insulin resistance (HOMA-IR). In these mice, serum concentrations of leukocyte cell–derived chemotaxin 2 (LECT2), which is known to induce insulin resistance in skeletal muscle, were elevated, and insulin signaling in muscle, as determined by the phosphorylation levels of Akt and p70 S6 kinases, tended to be decreased. In HFGT diet–fed mice, these signs of insulin resistance and elevation of serum LECT2 were not observed. Although our study did not directly show the effect of serum LECT2 on muscle weight, insulin resistance examined using HOMA-IR indicated an intervention effect of serum LECT2 on muscle weight, as revealed by partial correlation analysis. Accordingly, GTEs might have beneficial effects on age-related and HF diet–induced muscle weight loss, which correlates with insulin resistance and is accompanied by a change in serum LECT2.

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          Most cited references29

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          Signaling pathways controlling skeletal muscle mass

          The molecular mechanisms underlying skeletal muscle maintenance involve interplay between multiple signaling pathways. Under normal physiological conditions, a network of interconnected signals serves to control and coordinate hypertrophic and atrophic messages, culminating in a delicate balance between muscle protein synthesis and proteolysis. Loss of skeletal muscle mass, termed “atrophy”, is a diagnostic feature of cachexia seen in settings of cancer, heart disease, chronic obstructive pulmonary disease, kidney disease, and burns. Cachexia increases the likelihood of death from these already serious diseases. Recent studies have further defined the pathways leading to gain and loss of skeletal muscle as well as the signaling events that induce differentiation and post-injury regeneration, which are also essential for the maintenance of skeletal muscle mass. In this review, we summarize and discuss the relevant recent literature demonstrating these previously undiscovered mediators governing anabolism and catabolism of skeletal muscle.
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            A liver-derived secretory protein, selenoprotein P, causes insulin resistance.

            The liver may regulate glucose homeostasis by modulating the sensitivity/resistance of peripheral tissues to insulin, by way of the production of secretory proteins, termed hepatokines. Here, we demonstrate that selenoprotein P (SeP), a liver-derived secretory protein, causes insulin resistance. Using serial analysis of gene expression (SAGE) and DNA chip methods, we found that hepatic SeP mRNA levels correlated with insulin resistance in humans. Administration of purified SeP impaired insulin signaling and dysregulated glucose metabolism in both hepatocytes and myocytes. Conversely, both genetic deletion and RNA interference-mediated knockdown of SeP improved systemic insulin sensitivity and glucose tolerance in mice. The metabolic actions of SeP were mediated, at least partly, by inactivation of adenosine monophosphate-activated protein kinase (AMPK). In summary, these results demonstrate a role of SeP in the regulation of glucose metabolism and insulin sensitivity and suggest that SeP may be a therapeutic target for type 2 diabetes. Copyright © 2010 Elsevier Inc. All rights reserved.
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              Loss of muscle strength, mass (sarcopenia), and quality (specific force) and its relationship with functional limitation and physical disability: the Concord Health and Ageing in Men Project.

              To determine the association between loss of muscle strength, mass, and quality and functional limitation and physical disability in older men. Cross-sectional study of older men participating in the Concord Health and Ageing in Men Project (CHAMP). Elderly men living in a defined geographical region in Sydney, Australia. One thousand seven hundred five community-dwelling men aged 70 and older who participated in the baseline assessments of CHAMP. Upper and lower extremity strength were measured using dynamometers for grip and quadriceps strength. Appendicular skeletal lean mass was assessed using dual X-ray absorptiometry. Muscle quality was defined as the ratio of strength to mass in upper and lower extremities. For each parameter, subjects in the lowest 20% of the distribution were defined as below normal. Functional limitation was assessed according to self-report and objective lower extremity performance measures. Physical disability was measured according to self-report questionnaire. After adjusting for important confounders, the prevalence ratio (PR) for poor quadriceps strength and self-reported functional limitation was 1.91 (95% confidence interval (CI) = 1.10-2.40); for performance-based functional limitation the PR was 1.81 (95% CI = 1.45-2.24). The adjusted PR for poor grip strength and physical disability in instrumental activities of daily living (IADLs) was 1.37 (95% CI = 1.20-1.56). The adjusted PR for low skeletal lean mass (adjusted for fat mass) and physical disability in basic activities of daily living was 2.08 (95% CI = 1.37-3.15). For muscle quality, the PR for lower extremity specific force and functional limitation and physical disability was stronger than upper extremity specific force. Muscle strength is the single best measure of age-related muscle change and is associated with physical disability in IADLs and functional limitation. © 2010, Copyright the Authors. Journal compilation © 2010, The American Geriatrics Society.
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                Author and article information

                Contributors
                Role: ConceptualizationRole: Data curationRole: Formal analysisRole: InvestigationRole: MethodologyRole: Writing – original draftRole: Writing – review & editing
                Role: Data curationRole: Investigation
                Role: Data curationRole: InvestigationRole: Methodology
                Role: Investigation
                Role: Investigation
                Role: Investigation
                Role: ConceptualizationRole: Data curationRole: MethodologyRole: Project administrationRole: ResourcesRole: SupervisionRole: Writing – review & editing
                Role: ConceptualizationRole: Data curationRole: Formal analysisRole: MethodologyRole: Project administrationRole: Writing – original draftRole: Writing – review & editing
                Role: ConceptualizationRole: Data curationRole: MethodologyRole: Project administrationRole: ResourcesRole: SupervisionRole: Writing – review & editing
                Role: ConceptualizationRole: Data curationRole: MethodologyRole: Project administrationRole: ResourcesRole: SupervisionRole: Writing – review & editing
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                9 April 2018
                2018
                : 13
                : 4
                : e0195753
                Affiliations
                [1 ] Industry–Academia Collaboration Research Laboratory of the University of Shizuoka and Kao Corporation, University of Shizuoka, Shizuoka, Japan
                [2 ] Laboratory of Nutritional Biochemistry, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka, Japan
                [3 ] Department of Neurophysiology, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan
                East Tennessee State University, UNITED STATES
                Author notes

                Competing Interests: The authors have the following interests: This work was supported by industry-academia collaboration between the University of Shizuoka and Kao Corporation. There are no patents, products in development or marketed products to declare. This does not alter our adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.

                [¤a]

                Current address: Biological Science Research, Kao Corporation, Haga-gun, Tochigi, Japan

                [¤b]

                Current address: Department of Health and Food Science, University of Human Arts and Science, Saitama, Japan

                Author information
                http://orcid.org/0000-0001-6555-2541
                http://orcid.org/0000-0001-7995-2220
                http://orcid.org/0000-0002-3072-2632
                Article
                PONE-D-18-01676
                10.1371/journal.pone.0195753
                5891070
                29630667
                c7b2955a-fb04-4e4d-974b-9fd471f1ea79
                © 2018 Onishi et al

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 17 January 2018
                : 28 March 2018
                Page count
                Figures: 4, Tables: 4, Pages: 14
                Funding
                This work was supported by industry-academia collaboration between the University of Shizuoka and Kao Corporation. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Biology and Life Sciences
                Anatomy
                Musculoskeletal System
                Muscles
                Skeletal Muscles
                Medicine and Health Sciences
                Anatomy
                Musculoskeletal System
                Muscles
                Skeletal Muscles
                Biology and Life Sciences
                Nutrition
                Diet
                Medicine and Health Sciences
                Nutrition
                Diet
                Medicine and Health Sciences
                Endocrinology
                Endocrine Physiology
                Insulin Resistance
                Biology and Life Sciences
                Physiology
                Endocrine Physiology
                Insulin Resistance
                Medicine and Health Sciences
                Physiology
                Endocrine Physiology
                Insulin Resistance
                Medicine and Health Sciences
                Endocrinology
                Diabetic Endocrinology
                Insulin
                Biology and Life Sciences
                Biochemistry
                Hormones
                Insulin
                Medicine and Health Sciences
                Diagnostic Medicine
                Signs and Symptoms
                Atrophy
                Medicine and Health Sciences
                Pathology and Laboratory Medicine
                Signs and Symptoms
                Atrophy
                Medicine and Health Sciences
                Endocrinology
                Endocrine Physiology
                Insulin Signaling
                Biology and Life Sciences
                Physiology
                Endocrine Physiology
                Insulin Signaling
                Medicine and Health Sciences
                Physiology
                Endocrine Physiology
                Insulin Signaling
                Research and Analysis Methods
                Chemical Synthesis
                Biosynthetic Techniques
                Protein Synthesis
                Muscle Protein Synthesis
                Biology and Life Sciences
                Biochemistry
                Proteins
                Protein Synthesis
                Muscle Protein Synthesis
                Research and Analysis Methods
                Chemical Synthesis
                Biosynthetic Techniques
                Protein Synthesis
                Biology and Life Sciences
                Biochemistry
                Proteins
                Protein Synthesis
                Custom metadata
                All relevant data are within the paper and its Supporting Information files.

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