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      Exercise training to reduce cardiovascular risk in patients with metabolic syndrome and type 2 diabetes mellitus: How does it work?

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          Abstract

          Metabolic syndrome (MetS) - a clustering of pathological conditions, including abdominal obesity, hypertension, dyslipidemia and hyperglycaemia - is closely associated with the development of type 2 diabetes mellitus (T2DM) and a high risk of cardiovascular disease. A combination of multigenetic predisposition and lifestyle choices accounts for the varying inter-individual risk to develop MetS and T2DM, as well as for the individual amount of the increase in cardiovascular risk in those patients. A physically active lifestyle can offset about half of the genetically mediated cardiovascular risk. Yet, the extent to which standardized exercise programmes can reduce cardiovascular risk differs between patients. Exercise parameters, such as frequency, intensity, type and duration or number of repetitions, differentially target metabolic function, vascular health and physical fitness. In addition, exercise-induced molecular mechanisms are modulated by other patient-specific variables, such as age, diet and medication. This review discusses the molecular and cellular mechanisms underlying the effects of exercise training on cardiovascular risk specifically in patients with MetS and T2DM.

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          AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy.

          D Hardie (2007)
          The SNF1/AMP-activated protein kinase (AMPK) family maintains the balance between ATP production and consumption in all eukaryotic cells. The kinases are heterotrimers that comprise a catalytic subunit and regulatory subunits that sense cellular energy levels. When energy status is compromised, the system activates catabolic pathways and switches off protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. Surprisingly, recent results indicate that the AMPK system is also important in functions that go beyond the regulation of energy homeostasis, such as the maintenance of cell polarity in epithelial cells.
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            Reprogramming mitochondrial metabolism in macrophages as an anti-inflammatory signal.

            Evanna L Mills, Luke A. O’Neill (2016)
            Mitochondria are master regulators of metabolism. Mitochondria generate ATP by oxidative phosphorylation using pyruvate (derived from glucose and glycolysis) and fatty acids (FAs), both of which are oxidized in the Krebs cycle, as fuel sources. Mitochondria are also an important source of reactive oxygen species (ROS), creating oxidative stress in various contexts, including in the response to bacterial infection. Recently, complex changes in mitochondrial metabolism have been characterized in mouse macrophages in response to varying stimuli in vitro. In LPS and IFN-γ-activated macrophages (M1 macrophages), there is decreased respiration and a broken Krebs cycle, leading to accumulation of succinate and citrate, which act as signals to alter immune function. In IL-4-activated macrophages (M2 macrophages), the Krebs cycle and oxidative phosphorylation are intact and fatty acid oxidation (FAO) is also utilized. These metabolic alterations in response to the nature of the stimulus are proving to be determinants of the effector functions of M1 and M2 macrophages. Furthermore, reprogramming of macrophages from M1 to M2 can be achieved by targeting metabolic events. Here, we describe the role that metabolism plays in macrophage function in infection and immunity, and propose that reprogramming with metabolic inhibitors might be a novel therapeutic approach for the treatment of inflammatory diseases.
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              The transcriptional coactivator PGC-1alpha mediates exercise-induced angiogenesis in skeletal muscle.

              Stephen R Thom, Jessica Chinsomboon, Jorge L Ruas … (2009)
              Peripheral arterial disease (PAD) affects 5 million people in the US and is the primary cause of limb amputations. Exercise remains the single best intervention for PAD, in part thought to be mediated by increases in capillary density. How exercise triggers angiogenesis is not known. PPARgamma coactivator (PGC)-1alpha is a potent transcriptional co-activator that regulates oxidative metabolism in a variety of tissues. We show here that PGC-1alpha mediates exercise-induced angiogenesis. Voluntary exercise induced robust angiogenesis in mouse skeletal muscle. Mice lacking PGC-1alpha in skeletal muscle failed to increase capillary density in response to exercise. Exercise strongly induced expression of PGC-1alpha from an alternate promoter. The induction of PGC-1alpha depended on beta-adrenergic signaling. beta-adrenergic stimulation also induced a broad program of angiogenic factors, including vascular endothelial growth factor (VEGF). This induction required PGC-1alpha. The orphan nuclear receptor ERRalpha mediated the induction of VEGF by PGC-1alpha, and mice lacking ERRalpha also failed to increase vascular density after exercise. These data demonstrate that beta-adrenergic stimulation of a PGC-1alpha/ERRalpha/VEGF axis mediates exercise-induced angiogenesis in skeletal muscle.
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                Author and article information

                Journal
                Title: European Journal of Preventive Cardiology
                Abbreviated Title: Eur J Prev Cardiolog
                Publisher: SAGE Publications
                ISSN (Print): 2047-4873
                ISSN (Electronic): 2047-4881
                Publication date Created: October 15 2018
                Publication date (Electronic): October 15 2018
                Page: 204748731880515
                Affiliations
                [1 ]Charité – Universitätsmedizin Berlin, Klinik für Kardiologie, Campus Benjamin Steglitz, Berlin, Germany
                [2 ]DZHK (German Centre for Cardiovascular Research), Partner Site, Berlin, Germany
                [3 ]University Medicine Greifswald, Department of Internal Medicine B, Greifswald, Germany
                [4 ]DZHK (German Centre for Cardiovascular Research), Partner Site, Greifswald, Germany
                [5 ]Department of Cardiology, Antwerp University Hospital, Antwerp, Belgium
                [6 ]Department of Molecular and Experimental Cardiology, TU Dresden, Heart Centre Dresden, Dresden, Germany
                [7 ]Hospital Universitario Quironsalud, Madrid, Spain
                [8 ]Ripoll & De Prado Sport Clinic, FIFA Medical Centre of Excellence, Madrid, Spain
                [9 ]Diakonhjemmet hospital, Department of Medicine, Oslo, Norway
                [10 ]Hasselt University, Faculty of Rehabilitation Sciences, Diepenbeek, Belgium
                [11 ]Heart Centre Hasselt, Jessa Hospital, Hasselt, Belgium
                [12 ]Department of Cardiology, Máxima Medical Centre, Veldhoven, The Netherlands
                Article
                DOI: 10.1177/2047487318805158
                SO-VID: 2bcb9519-9957-4a62-9a57-2be202887f1b
                Copyright © © 2018
                License:

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

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