Seyed Reza Mirhafez1, Mohammad Tajfard2, Amir Avan2, Alireza Pasdar3, Reza Nedaeinia4, Malihe Aghasizade2, Hafezeh Davari2, Mostafa Manian5, Adeleh Mahdizadeh6, Zahra Meshkat7, Ali Movahedi8, Nahid Ghaed Amini9, Nahid Eskandari10, Rasoul Salehi11, Gordon A Ferns12, Majid Ghayour-Mobarhan13. 1. Department of Basic Medical Sciences, Neyshabur University of Medical Sciences, Neyshabur, Iran; Department of Modern Sciences and Technologies, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 2. Department of Modern Sciences and Technologies, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 3. Department of Modern Sciences and Technologies, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Division of Applied Medicine, Medical School, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK. 4. Student Research Committee, Department of Medical Biotechnology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Department of Microbiology, Deputy of Food and Drug, Isfahan University of Medical Sciences, Isfahan, Iran. 5. Immunology Research Center, Iran University of Medical Sciences, Tehran, Iran; Neurosciences Research Center, Alzahra Hospital, Isfahan University of Medical Sciences, Isfahan, Iran. 6. Cardiovascular Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 7. Antimicrobial Resistance Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. 8. Department of Basic Medical Sciences, Neyshabur University of Medical Sciences, Neyshabur, Iran. 9. Department of Biology, Payame Noor University of isfahan, Isfahan, Iran. 10. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Applied Physiology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. 11. Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. 12. Brighton & Sussex Medical School, Division of Medical Education, Falmer, Brighton, Sussex BN1 9PH, UK. 13. Biochemistry of Nutrition Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: ghayourm@mums.ac.ir.
Abstract
OBJECTIVE: Hypertriglyceridemia is an established risk factor for coronary-heart-disease. Inflammatory cytokines are known to be important mediators of atherogenesis; however, the relationship between the concentrations of specific inflammatory cytokines and the presence of hypertriglyceridemia has not been well established. The purpose of this study was to investigate the relationship between the serum levels of several pro- and anti-inflammatory cytokines and the presence of hypertriglyceridemia. DESIGN AND METHODS: Four hundred and eighty-four subjects with/without established hypertriglyceridemia were recruited. Anthropometric parameters and biochemical analysis (including a full fasting lipid profile) were determined. The serum levels of several cytokines and growth factors including IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, TNF-α, MCP-1, IFN-γ, EGF, and VEGF were measured followed by univariate and multivariate analyses. RESULTS: Individuals with hypertriglyceridemia had a significantly higher body mass index, total-cholesterol and triglyceride, compared to the group without hypertriglyceridemia. Serum levels of MCP-1, TNF-α and IL-8 were significantly higher in subjects with hypertriglyceridemia [e.g., IL-8 from 7.8ng/L (95% CI: 4.6-18.9) versus 5.7ng/L (95% CI: 3.6-11.9), P<0.05]. The multivariate analysis showed that the increased serum concentration of TNF-α was independently associated with high-density lipoprotein cholesterol (HDL-C), while the serum levels of IL-8 and MCP-1 were associated with hypertriglyceridemia. CONCLUSION: Subjects with serum triglycerides of ≥2.25mmol/L had an altered cytokine-profile, particularly with respect to serum IL-8, MCP-1 and TNF-α, which might partially account for its adverse clinical-consequences. Further-investigations in a large multi-center setting are warranted to unravel the potential functional-importance of these cytokines in individuals with hypertriglyceridemia.
OBJECTIVE:Hypertriglyceridemia is an established risk factor for coronary-heart-disease. Inflammatory cytokines are known to be important mediators of atherogenesis; however, the relationship between the concentrations of specific inflammatory cytokines and the presence of hypertriglyceridemia has not been well established. The purpose of this study was to investigate the relationship between the serum levels of several pro- and anti-inflammatory cytokines and the presence of hypertriglyceridemia. DESIGN AND METHODS: Four hundred and eighty-four subjects with/without established hypertriglyceridemia were recruited. Anthropometric parameters and biochemical analysis (including a full fasting lipid profile) were determined. The serum levels of several cytokines and growth factors including IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, TNF-α, MCP-1, IFN-γ, EGF, and VEGF were measured followed by univariate and multivariate analyses. RESULTS: Individuals with hypertriglyceridemia had a significantly higher body mass index, total-cholesterol and triglyceride, compared to the group without hypertriglyceridemia. Serum levels of MCP-1, TNF-α and IL-8 were significantly higher in subjects with hypertriglyceridemia [e.g., IL-8 from 7.8ng/L (95% CI: 4.6-18.9) versus 5.7ng/L (95% CI: 3.6-11.9), P<0.05]. The multivariate analysis showed that the increased serum concentration of TNF-α was independently associated with high-density lipoprotein cholesterol (HDL-C), while the serum levels of IL-8 and MCP-1 were associated with hypertriglyceridemia. CONCLUSION: Subjects with serum triglycerides of ≥2.25mmol/L had an altered cytokine-profile, particularly with respect to serum IL-8, MCP-1 and TNF-α, which might partially account for its adverse clinical-consequences. Further-investigations in a large multi-center setting are warranted to unravel the potential functional-importance of these cytokines in individuals with hypertriglyceridemia.
Authors: Josiane B S Braun; Jader B Ruchel; Alessandra G Manzoni; Fátima H Abdalla; Emerson A Casalli; Lívia G Castilhos; Daniela F Passos; Daniela B R Leal Journal: Mol Cell Biochem Date: 2017-11-29 Impact factor: 3.396