Effects of Moderate Exercise Training On ApoE And ApoCIII In Metabolic Syndrome


Abstract views: 171 / PDF downloads: 130

Authors

DOI:

https://doi.org/10.58600/eurjther-184

Keywords:

Adipokines, Apolioprotein CIII, Apolipoprotein, exercise, metabolic syndrome

Abstract

Introduction: Metabolic syndrome (MetS) is an endocrinopathy with a combination of cardiovascular and metabolic compounds. In our study, it is expected to obtain results showing that mortality rate, loss of workforce, and treatment costs due to disorders caused by MetS can be reduced by physical exercise. The study analyses the effect of moderate exercise training on this Apolipoprotein E (ApoE), Apolipoprotein CIII (ApoCIII), adiponectin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) which are thought to have a role in the deterioration of glucose and lipid metabolism in MetS.

Methods: This clinical experimental study consists of 3 groups. The MetS+E (n=24) group, which included the participants who agreed to participate in the exercise program in addition to their medical treatment, the MetS (n=23) group who received medical treatment but did not exercise, and the Control+E (n=25) group, which included healthy volunteers who had the same protocol as MetS+E ApoE, ApoCIII, adiponectin, resistin, IL-6, and TNF-α plasma levels of all participants were measured both at the beginning of the study and at the end of the protocol.

Results: At the end of the study we reached the following findings; insulin and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) levels decreased in exercise groups (p=0,03). ApoCIII levels increased in all the groups after the study (p<0,01). IL-6 levels decreased in MetS+E (p<0,01) and Control+E (p=0,037). ApoE (p=0,01) and TNF-α (p=0,037) levels decreased only in the Control+E group.

Conclusion: Training showed metabolic, anti-inflammatory, and physical improvements independent of ApoE and ApoCIII in those with MetS.

Metrics

Metrics Loading ...

References

Chaldakov, George N. Obesity: an inside versus outside view Jimmy Bell and the Little Prince A science-in-fiction dedicated to World Obesity Day 2017. Scripta Scientifica Vox Studentium, 2017; 1.1: 13-17.

Reaven, Gerald M. Role of insulin resistance in human disease. Diabetes, 1988; 37.12: 1595-1607.

Craig, Cora L., et al. International physical activity questionnaire: 12-country reliability and validity. Medicine and science in sports and exercise, 2003; 35.8: 1381-1395.

Matthews, David R., et al. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia, 1985; 28.7: 412-419.

Hill, Jonathan; TIMMIS, Adam. Exercise tolerance testing. Bmj, 2002; 324.7345: 1084-1087.

Arner, Peter. Catecholamine-induced lipolysis in obesity. International Journal of Obesity, 1999; 23.1: S10-S13.

Achten, J., Asker, VM.. Maximal Fat Oxidation During Exercise in Trained Men. International journal of sports medicine. 2003; 24. 603-608.

Kim, Dae-Young; SEO, Byoung-Do; KIM, Dong-Je. Effect of walking exercise on changes in cardiorespiratory fitness, metabolic syndrome markers, and high-molecular-weight adiponectin in obese middle-aged women. Journal of physical therapy science, 2014; 26.11: 1723-1727.

Achten, J., Asker, VM Fat Oxidation Rates Are Higher During Running Compared With Cycling Over a Wide Range of Intensities. Metabolism: clinical and experimental. 2003;52:747-752.

Hara, Taketaka, et al. Body composition is related to increase in plasma adiponectin levels rather than training in young obese men. European journal of applied physiology, 2005; 94.5: 520-526.

Giannopoulou, Ifigenia, et al. Effects of diet and/or exercise on the adipocytokine and inflammatory cytokine levels of postmenopausal women with type 2 diabetes. Metabolism, 2005; 54.7: 866-875.

Hotamisligil, Gökhan S., et al. IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-α-and obesity-induced insulin resistance. Science, 1996; 271.5249: 665-670.

Wood, I. Stuart, et al. Cellular hypoxia and adipose tissue dysfunction in obesity: symposium on ‘Frontiers in Adipose Tissue Biology’. Proceedings of the Nutrition Society, 2009; 68.4: 370-377.

Brunmair, Barbara, et al. Thiazolidinediones, like metformin, inhibit respiratory complex I: a common mechanism contributing to their antidiabetic actions?. Diabetes, 2004; 53.4: 1052-1059.

Boiko, Anastasiia S., et al. Apolipoprotein serum levels related to metabolic syndrome in patients with schizophrenia. Heliyon, 2019; 5.7: e02033.

Shiina, Yutaka; Homma, Yasuhiko. Relationships between the visceral fat area on CT and coronary risk factor markers. Internal Medicine, 2013; 52.16: 1775-1780.

Onat, Altan, et al. High serum apolipoprotein E determines hypertriglyceridemic dyslipidemias, coronary disease and apoA‐I dysfunctionality. Lipids, 2013; 48.1: 51-61.

Onat, Altan; Can, Günay; Yüksel, Hüsniye. Dysfunction of high-density lipoprotein and its apolipoproteins: new mechanisms underlying cardiometabolic risk in the population at large. Turk Kardiyol Dern Ars, 2012; 40.4: 368-85.

Lai, Lana YH, et al. Lack of association of apolipoprotein E (Apo E) polymorphism with the prevalence of metabolic syndrome: the National Heart, Lung and Blood Institute Family Heart Study. Diabetes/metabolism research and reviews, 2015; 31.6: 582-587.

Son, Ki Young, et al. Genetic association of APOA5 and APOE with metabolic syndrome and their interaction with health-related behavior in Korean men. Lipids in health and disease, 2015; 14.1: 1-9.

Reas, Emilie T., et al. Effects of APOE on cognitive aging in community-dwelling older adults. Neuropsychology, 2019; 33.3: 406.

Brown, Dawson; GIBAS, Kelly J. Metabolic syndrome marks early risk for cognitive decline with APOE4 gene variation: A case study. Diabetes & Metabolic Syndrome: Clinical Research & Reviews, 2018; 12.5: 823-827.

Sparks, D. L.; Prıtchard, P. H. Transfer of cholesteryl ester into high density lipoprotein by cholesteryl ester transfer protein: effect of HDL lipid and apoprotein content. Journal of Lipid Research, 1989; 30.10: 1491-1498.

Towle, Howard C. Glucose as a regulator of eukaryotic gene transcription. Trends in Endocrinology & Metabolism, 2005; 16.10: 489-494.

Caron, Sandrine, et al. Transcriptional activation of apolipoprotein CIII expression by glucose may contribute to diabetic dyslipidemia. Arteriosclerosis, thrombosis, and vascular biology, 2011; 31.3: 513-519.

Ginsberg, Henry N.; Brown, W. Virgil. Apolipoprotein CIII: 42 years old and even more interesting. Arteriosclerosis, thrombosis, and vascular biology, 2011; 31.3: 471-473.

Wang, Wenyu, et al. Apolipoproteins AI, B, and C-III in young adult Cherokee with metabolic syndrome with or without type 2 diabetes. Journal of clinical lipidology, 2013; 7.1: 38-42.

Kremen, Jaromir, et al. Increased subcutaneous and epicardial adipose tissue production of proinflammatory cytokines in cardiac surgery patients: possible role in postoperative insulin resistance. The journal of clinical endocrinology & metabolism, 2006; 91.11: 4620-4627.

Balducci, Stefano, et al. Anti-inflammatory effect of exercise training in subjects with type 2 diabetes and the metabolic syndrome is dependent on exercise modalities and independent of weight loss. Nutrition, Metabolism and Cardiovascular Diseases, 2010; 20.8: 608-617.

Srikanthan, Krithika, et al. Systematic review of metabolic syndrome biomarkers: a panel for early detection, management, and risk stratification in the West Virginian population. International journal of medical sciences, 2016; 13.1: 25.

Downloads

Published

2023-03-30

How to Cite

Ertekin, K., Baştuğ, M., & Gökçay Canpolat, A. (2023). Effects of Moderate Exercise Training On ApoE And ApoCIII In Metabolic Syndrome. European Journal of Therapeutics, 29(1), 65–73. https://doi.org/10.58600/eurjther-184

Issue

Section

Original Articles