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      Benefits of Physical Activity on Cardiometabolic Diseases in Obese Children and Adolescents

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          Abstract

          In the past few decades, obesity in the pediatric population has dramatically increased and is common in many countries. Childhood obesity often causes health problems and increases the risk of cardiometabolic diseases such as type 2 diabetes, nonalcohol fatty liver, and cardiovascular diseases. Obesity in young people has been closely associated with environmental, behavioral, and genetic defects, including the availability of high-energy and sugary food and beverages, sedentary behavior, and hereditary factors. Few drugs are currently available to treat obesity in children and adolescents because it is difficult to demonstrate the safety of these drugs on the growth and development of the youth. Lifestyle modifications, such as diet control and physical exercise, are the primary approaches for preventing and treating childhood obesity. Among them, physical activity is a crucial component. This review summarizes the epidemiology, cardiometabolic risk of obesity, therapeutic strategies, and the benefits of exercise on obesity-related chronic diseases in children and adolescents.

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          Most cited references80

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          The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology.

          For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phagocyte NADPH oxidase were found: NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2. Together with the phagocyte NADPH oxidase itself (NOX2/gp91(phox)), the homologs are now referred to as the NOX family of NADPH oxidases. These enzymes share the capacity to transport electrons across the plasma membrane and to generate superoxide and other downstream reactive oxygen species (ROS). Activation mechanisms and tissue distribution of the different members of the family are markedly different. The physiological functions of NOX family enzymes include host defense, posttranlational processing of proteins, cellular signaling, regulation of gene expression, and cell differentiation. NOX enzymes also contribute to a wide range of pathological processes. NOX deficiency may lead to immunosuppresion, lack of otoconogenesis, or hypothyroidism. Increased NOX activity also contributes to a large number or pathologies, in particular cardiovascular diseases and neurodegeneration. This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.
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            Mechanisms linking obesity to insulin resistance and type 2 diabetes.

            Obesity is associated with an increased risk of developing insulin resistance and type 2 diabetes. In obese individuals, adipose tissue releases increased amounts of non-esterified fatty acids, glycerol, hormones, pro-inflammatory cytokines and other factors that are involved in the development of insulin resistance. When insulin resistance is accompanied by dysfunction of pancreatic islet beta-cells - the cells that release insulin - failure to control blood glucose levels results. Abnormalities in beta-cell function are therefore critical in defining the risk and development of type 2 diabetes. This knowledge is fostering exploration of the molecular and genetic basis of the disease and new approaches to its treatment and prevention.
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              Increased oxidative stress in obesity and its impact on metabolic syndrome.

              Obesity is a principal causative factor in the development of metabolic syndrome. Here we report that increased oxidative stress in accumulated fat is an important pathogenic mechanism of obesity-associated metabolic syndrome. Fat accumulation correlated with systemic oxidative stress in humans and mice. Production of ROS increased selectively in adipose tissue of obese mice, accompanied by augmented expression of NADPH oxidase and decreased expression of antioxidative enzymes. In cultured adipocytes, elevated levels of fatty acids increased oxidative stress via NADPH oxidase activation, and oxidative stress caused dysregulated production of adipocytokines (fat-derived hormones), including adiponectin, plasminogen activator inhibitor-1, IL-6, and monocyte chemotactic protein-1. Finally, in obese mice, treatment with NADPH oxidase inhibitor reduced ROS production in adipose tissue, attenuated the dysregulation of adipocytokines, and improved diabetes, hyperlipidemia, and hepatic steatosis. Collectively, our results suggest that increased oxidative stress in accumulated fat is an early instigator of metabolic syndrome and that the redox state in adipose tissue is a potentially useful therapeutic target for obesity-associated metabolic syndrome.
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                Author and article information

                Journal
                J Transl Int Med
                J Transl Int Med
                jtim
                Journal of Translational Internal Medicine
                Sciendo
                2450-131X
                2224-4018
                September 2022
                30 September 2022
                : 10
                : 3
                : 236-245
                Affiliations
                [1 ]Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People’s Hospital of Nantong), School of Medicine, Shanghai University , Nantong 226011, Jiangsu Province, China
                [2 ]Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, School of Life Science, Shanghai University , Shanghai 200444, China
                [3 ]Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School , Boston 02114, MA, USA
                [4 ]Institute of Biochemistry and Cellular Biology, National Research Council of Italy , Napoli 80131, Italy
                Author notes

                Website: www.intern-med.com

                #These authors contributed equally to this work.

                [* ] Prof. Junjie Xiao, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People’s Hospital of Nantong), School of Medicine, Shanghai University, No. 881 Yonghe Road, Nantong 226011, Jiangsu Province, China. Junjiexiao@ 123456shu.edu.cn
                Article
                jtim-2022-0041
                10.2478/jtim-2022-0041
                9901555
                36776239
                37472344-01e3-4b3f-8d02-9f152aa0f70a
                © 2022 Juan Gao, Yi Lu, Priyanka Gokulnath, Gururaja Vulugundam, Guoping Li, Jin Li, Junjie Xiao, published by Sciendo

                This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

                History
                Page count
                Pages: 10
                Funding
                This work was supported by the National Key R&D Program of China (No. 2020YFA0803800 to Li J), National Natural Science Foundation of China (No. 82020108002 and 81911540486 to Xiao J, No. 82170390 to Gao J), the grant from Science and Technology Commission of Shanghai Municipality (No. 20DZ2255400 and 21XD1421300 to Xiao J, No. 21ZR1422700 to Gao J), and the “Dawn” Program of Shanghai Education Commission (No. 19SG34 to Xiao J).
                Categories
                Review Article

                pediatric obesity,cardiometabolic diseases,sedentary behavior,lifestyle modification,physical exercise

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