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      Diabetic myopathy: impact of diabetes mellitus on skeletal muscle progenitor cells

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          Abstract

          Diabetes mellitus is defined as a group of metabolic diseases that are associated with the presence of a hyperglycemic state due to impairments in insulin release and/or function. While the development of each form of diabetes (Type 1 or Type 2) drastically differs, resultant pathologies often overlap. In each diabetic condition, a failure to maintain healthy muscle is often observed, and is termed diabetic myopathy. This significant, but often overlooked, complication is believed to contribute to the progression of additional diabetic complications due to the vital importance of skeletal muscle for our physical and metabolic well-being. While studies have investigated the link between changes to skeletal muscle metabolic health following diabetes mellitus onset (particularly Type 2 diabetes mellitus), few have examined the negative impact of diabetes mellitus on the growth and reparative capacities of skeletal muscle that often coincides with disease development. Importantly, evidence is accumulating that the muscle progenitor cell population (particularly the muscle satellite cell population) is also negatively affected by the diabetic environment, and as such, likely contributes to the declining skeletal muscle health observed in diabetes mellitus. In this review, we summarize the current knowledge surrounding the influence of diabetes mellitus on skeletal muscle growth and repair, with a particular emphasis on the impact of diabetes mellitus on skeletal muscle progenitor cell populations.

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          Satellite cells are essential for skeletal muscle regeneration: the cell on the edge returns centre stage.

          Following their discovery in 1961, it was speculated that satellite cells were dormant myoblasts, held in reserve until required for skeletal muscle repair. Evidence for this accumulated over the years, until the link between satellite cells and the myoblasts that appear during muscle regeneration was finally established. Subsequently, it was demonstrated that, when grafted, satellite cells could also self-renew, conferring on them the coveted status of 'stem cell'. The emergence of other cell types with myogenic potential, however, questioned the precise role of satellite cells. Here, we review recent recombination-based studies that have furthered our understanding of satellite cell biology. The clear consensus is that skeletal muscle does not regenerate without satellite cells, confirming their pivotal and non-redundant role.
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            The effect of insulin on the disposal of intravenous glucose. Results from indirect calorimetry and hepatic and femoral venous catheterization.

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              Myogenic satellite cells: physiology to molecular biology.

              Adult skeletal muscle has a remarkable ability to regenerate following myotrauma. Because adult myofibers are terminally differentiated, the regeneration of skeletal muscle is largely dependent on a small population of resident cells termed satellite cells. Although this population of cells was identified 40 years ago, little is known regarding the molecular phenotype or regulation of the satellite cell. The use of cell culture techniques and transgenic animal models has improved our understanding of this unique cell population; however, the capacity and potential of these cells remain ill-defined. This review will highlight the origin and unique markers of the satellite cell population, the regulation by growth factors, and the response to physiological and pathological stimuli. We conclude by highlighting the potential therapeutic uses of satellite cells and identifying future research goals for the study of satellite cell biology.
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                Author and article information

                Journal
                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                1664-042X
                20 November 2013
                20 December 2013
                2013
                : 4
                : 379
                Affiliations
                Department of Pathology and Molecular Medicine, McMaster University Hamilton, ON, Canada
                Author notes

                Edited by: Lucas Guimarães-Ferreira, Federal University of Espirito Santo, Brazil

                Reviewed by: Espen Spangenburg, University of Maryland, USA; Carlos H. J. Pinheiro, University of São Paulo, Brazil; Rebecca Berdeaux, University of Texas Health Science Center at Houston, USA

                *Correspondence: Thomas J. Hawke, Department of Pathology and Molecular Medicine, McMaster University, 1280 Main Street West, Hamilton, ON L8S 4L8, Canada e-mail: hawke@ 123456mcmaster.ca

                This article was submitted to Striated Muscle Physiology, a section of the journal Frontiers in Physiology.

                Article
                10.3389/fphys.2013.00379
                3868943
                24391596
                f18d7d2c-6fa6-44e8-bff8-13d6e0decbef
                Copyright © 2013 D'Souza, Al-Sajee and Hawke.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 31 October 2013
                : 04 December 2013
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 100, Pages: 7, Words: 6731
                Categories
                Physiology
                Mini Review Article

                Anatomy & Physiology
                diabetes mellitus,skeletal muscle,type 2 diabetes mellitus,muscle satellite cells,pics,muscle regeneration,type 1 diabetes mellitus

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