Effect of a short-term diet and exercise intervention on oxidative stress, inflammation, MMP-9, and monocyte chemotactic activity in men with metabolic syndrome factors
1 Department of Physiological Science, University of California, Los Angeles; 2 Division of Endocrinology, Metabolism and Molecular Medicine, Charles R. Drew University, Los Angeles; and 3 Division of Nephrology and Hypertension, Department of Medicine, University of California, Irvine, California S...
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Published in | Journal of applied physiology (1985) Vol. 100; no. 5; pp. 1657 - 1665 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Bethesda, MD
Am Physiological Soc
01.05.2006
American Physiological Society |
Subjects | |
Online Access | Get full text |
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Abstract | 1 Department of Physiological Science, University of California, Los Angeles; 2 Division of Endocrinology, Metabolism and Molecular Medicine, Charles R. Drew University, Los Angeles; and 3 Division of Nephrology and Hypertension, Department of Medicine, University of California, Irvine, California
Submitted 6 October 2005
; accepted in final form 14 December 2005
ABSTRACT
The present study was designed to examine the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress, inflammation, chemotaxis, and cell adhesion. Obese men ( n = 31), 15 of whom had metabolic syndrome, were placed on a high-fiber, low-fat diet in a 3-wk residential program where food was provided ad libitum and daily aerobic exercise was performed. In each subject, pre- and postintervention fasting blood was drawn for circulating levels of serum lipids, glucose and insulin (for estimation of insulin sensitivity), oxidative stress-generating enzyme myeloperoxidase and marker 8-isoprostaglandin F 2 , the inflammatory protein C-reactive protein, soluble ICAM-1 as an indicator of endothelial activation, sP-selectin as a marker of platelet activation, the chemokine macrophage inflammatory protein-1 , and total matrix metalloproteinase-9. Using subject sera and human aortic endothelial cell culture systems, we measured VCAM-1 cell surface abundance and monocyte chemotactic protein-1, nitric oxide, superoxide, and hydrogen peroxide production in vitro by fluorometric detection. Also determined in vitro was serum-induced, monocyte adhesion and monocyte chemotactic activity. After 3 wk, significant reductions ( P < 0.05) in body mass index, all serum lipids and lipid ratios, fasting glucose, insulin, homeostasis model assessment for insulin resistance, myeloperoxidase, 8-isoprostaglandin F 2 , C-reactive protein, soluble ICAM-1, soluble P-selectin, macrophage inflammatory protein-1 , and matrix metalloproteinase-9 were noted. In vitro, serum-stimulated cellular VCAM-1 expression, monocyte chemotactic protein-1 production, and fluorometric detection of superoxide and hydrogen peroxide production decreased, whereas a concomitant increase in NO production was noted (all P < 0.01). Additionally, both monocyte adhesion ( P < 0.05) and MCA ( P < 0.01) decreased. Nine of 15 were no longer positive for metabolic syndrome postintervention. Intensive lifestyle modification may ameliorate novel coronary artery disease risk factors in men with metabolic syndrome factors before reversal of obesity.
atherosclerosis; lipids; cell adhesion molecules; nitric oxide; matrix metalloproteinase-9
Address for reprint requests and other correspondence: C. K. Roberts, Dept. of Physiological Science, UCLA, 4101 Life Sciences Bldg. 621 Charles E. Young Dr. South, Los Angeles, CA 90095-1606 (e-mail: croberts{at}ucla.edu ) |
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AbstractList | The present study was designed to examine the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress, inflammation, chemotaxis, and cell adhesion. Obese men ( n = 31), 15 of whom had metabolic syndrome, were placed on a high-fiber, low-fat diet in a 3-wk residential program where food was provided ad libitum and daily aerobic exercise was performed. In each subject, pre- and postintervention fasting blood was drawn for circulating levels of serum lipids, glucose and insulin (for estimation of insulin sensitivity), oxidative stress-generating enzyme myeloperoxidase and marker 8-isoprostaglandin F
2α
, the inflammatory protein C-reactive protein, soluble ICAM-1 as an indicator of endothelial activation, sP-selectin as a marker of platelet activation, the chemokine macrophage inflammatory protein-1α, and total matrix metalloproteinase-9. Using subject sera and human aortic endothelial cell culture systems, we measured VCAM-1 cell surface abundance and monocyte chemotactic protein-1, nitric oxide, superoxide, and hydrogen peroxide production in vitro by fluorometric detection. Also determined in vitro was serum-induced, monocyte adhesion and monocyte chemotactic activity. After 3 wk, significant reductions ( P < 0.05) in body mass index, all serum lipids and lipid ratios, fasting glucose, insulin, homeostasis model assessment for insulin resistance, myeloperoxidase, 8-isoprostaglandin F
2α
, C-reactive protein, soluble ICAM-1, soluble P-selectin, macrophage inflammatory protein-1α, and matrix metalloproteinase-9 were noted. In vitro, serum-stimulated cellular VCAM-1 expression, monocyte chemotactic protein-1 production, and fluorometric detection of superoxide and hydrogen peroxide production decreased, whereas a concomitant increase in NO production was noted (all P < 0.01). Additionally, both monocyte adhesion ( P < 0.05) and MCA ( P < 0.01) decreased. Nine of 15 were no longer positive for metabolic syndrome postintervention. Intensive lifestyle modification may ameliorate novel coronary artery disease risk factors in men with metabolic syndrome factors before reversal of obesity. 1 Department of Physiological Science, University of California, Los Angeles; 2 Division of Endocrinology, Metabolism and Molecular Medicine, Charles R. Drew University, Los Angeles; and 3 Division of Nephrology and Hypertension, Department of Medicine, University of California, Irvine, California Submitted 6 October 2005 ; accepted in final form 14 December 2005 ABSTRACT The present study was designed to examine the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress, inflammation, chemotaxis, and cell adhesion. Obese men ( n = 31), 15 of whom had metabolic syndrome, were placed on a high-fiber, low-fat diet in a 3-wk residential program where food was provided ad libitum and daily aerobic exercise was performed. In each subject, pre- and postintervention fasting blood was drawn for circulating levels of serum lipids, glucose and insulin (for estimation of insulin sensitivity), oxidative stress-generating enzyme myeloperoxidase and marker 8-isoprostaglandin F 2 , the inflammatory protein C-reactive protein, soluble ICAM-1 as an indicator of endothelial activation, sP-selectin as a marker of platelet activation, the chemokine macrophage inflammatory protein-1 , and total matrix metalloproteinase-9. Using subject sera and human aortic endothelial cell culture systems, we measured VCAM-1 cell surface abundance and monocyte chemotactic protein-1, nitric oxide, superoxide, and hydrogen peroxide production in vitro by fluorometric detection. Also determined in vitro was serum-induced, monocyte adhesion and monocyte chemotactic activity. After 3 wk, significant reductions ( P < 0.05) in body mass index, all serum lipids and lipid ratios, fasting glucose, insulin, homeostasis model assessment for insulin resistance, myeloperoxidase, 8-isoprostaglandin F 2 , C-reactive protein, soluble ICAM-1, soluble P-selectin, macrophage inflammatory protein-1 , and matrix metalloproteinase-9 were noted. In vitro, serum-stimulated cellular VCAM-1 expression, monocyte chemotactic protein-1 production, and fluorometric detection of superoxide and hydrogen peroxide production decreased, whereas a concomitant increase in NO production was noted (all P < 0.01). Additionally, both monocyte adhesion ( P < 0.05) and MCA ( P < 0.01) decreased. Nine of 15 were no longer positive for metabolic syndrome postintervention. Intensive lifestyle modification may ameliorate novel coronary artery disease risk factors in men with metabolic syndrome factors before reversal of obesity. atherosclerosis; lipids; cell adhesion molecules; nitric oxide; matrix metalloproteinase-9 Address for reprint requests and other correspondence: C. K. Roberts, Dept. of Physiological Science, UCLA, 4101 Life Sciences Bldg. 621 Charles E. Young Dr. South, Los Angeles, CA 90095-1606 (e-mail: croberts{at}ucla.edu ) The present study was designed to examine the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress, inflammation, chemotaxis, and cell adhesion. Obese men (n = 31), 15 of whom had metabolic syndrome, were placed on a high-fiber, low-fat diet in a 3-wk residential program where food was provided ad libitum and daily aerobic exercise was performed. In each subject, pre- and postintervention fasting blood was drawn for circulating levels of serum lipids, glucose and insulin (for estimation of insulin sensitivity), oxidative stress-generating enzyme myeloperoxidase and marker 8-isoprostaglandin F2alpha, the inflammatory protein C-reactive protein, soluble ICAM-1 as an indicator of endothelial activation, sP-selectin as a marker of platelet activation, the chemokine macrophage inflammatory protein-1alpha, and total matrix metalloproteinase-9. Using subject sera and human aortic endothelial cell culture systems, we measured VCAM-1 cell surface abundance and monocyte chemotactic protein-1, nitric oxide, superoxide, and hydrogen peroxide production in vitro by fluorometric detection. Also determined in vitro was serum-induced, monocyte adhesion and monocyte chemotactic activity. After 3 wk, significant reductions (P < 0.05) in body mass index, all serum lipids and lipid ratios, fasting glucose, insulin, homeostasis model assessment for insulin resistance, myeloperoxidase, 8-isoprostaglandin F2alpha, C-reactive protein, soluble ICAM-1, soluble P-selectin, macrophage inflammatory protein-1alpha, and matrix metalloproteinase-9 were noted. In vitro, serum-stimulated cellular VCAM-1 expression, monocyte chemotactic protein-1 production, and fluorometric detection of superoxide and hydrogen peroxide production decreased, whereas a concomitant increase in NO production was noted (all P < 0.01). Additionally, both monocyte adhesion (P < 0.05) and MCA (P < 0.01) decreased. Nine of 15 were no longer positive for metabolic syndrome postintervention. Intensive lifestyle modification may ameliorate novel coronary artery disease risk factors in men with metabolic syndrome factors before reversal of obesity.The present study was designed to examine the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress, inflammation, chemotaxis, and cell adhesion. Obese men (n = 31), 15 of whom had metabolic syndrome, were placed on a high-fiber, low-fat diet in a 3-wk residential program where food was provided ad libitum and daily aerobic exercise was performed. In each subject, pre- and postintervention fasting blood was drawn for circulating levels of serum lipids, glucose and insulin (for estimation of insulin sensitivity), oxidative stress-generating enzyme myeloperoxidase and marker 8-isoprostaglandin F2alpha, the inflammatory protein C-reactive protein, soluble ICAM-1 as an indicator of endothelial activation, sP-selectin as a marker of platelet activation, the chemokine macrophage inflammatory protein-1alpha, and total matrix metalloproteinase-9. Using subject sera and human aortic endothelial cell culture systems, we measured VCAM-1 cell surface abundance and monocyte chemotactic protein-1, nitric oxide, superoxide, and hydrogen peroxide production in vitro by fluorometric detection. Also determined in vitro was serum-induced, monocyte adhesion and monocyte chemotactic activity. After 3 wk, significant reductions (P < 0.05) in body mass index, all serum lipids and lipid ratios, fasting glucose, insulin, homeostasis model assessment for insulin resistance, myeloperoxidase, 8-isoprostaglandin F2alpha, C-reactive protein, soluble ICAM-1, soluble P-selectin, macrophage inflammatory protein-1alpha, and matrix metalloproteinase-9 were noted. In vitro, serum-stimulated cellular VCAM-1 expression, monocyte chemotactic protein-1 production, and fluorometric detection of superoxide and hydrogen peroxide production decreased, whereas a concomitant increase in NO production was noted (all P < 0.01). Additionally, both monocyte adhesion (P < 0.05) and MCA (P < 0.01) decreased. Nine of 15 were no longer positive for metabolic syndrome postintervention. Intensive lifestyle modification may ameliorate novel coronary artery disease risk factors in men with metabolic syndrome factors before reversal of obesity. The present study was designed to examine the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress, inflammation, chemotaxis, and cell adhesion. Obese men (n = 31), 15 of whom had metabolic syndrome, were placed on a high-fiber, low-fat diet in a 3-wk residential program where food was provided ad libitum and daily aerobic exercise was performed. In each subject, pre- and postintervention fasting blood was drawn for circulating levels of serum lipids, glucose and insulin (for estimation of insulin sensitivity), oxidative stress-generating enzyme myeloperoxidase and marker 8-isoprostaglandin F2alpha, the inflammatory protein C-reactive protein, soluble ICAM-1 as an indicator of endothelial activation, sP-selectin as a marker of platelet activation, the chemokine macrophage inflammatory protein-1alpha, and total matrix metalloproteinase-9. Using subject sera and human aortic endothelial cell culture systems, we measured VCAM-1 cell surface abundance and monocyte chemotactic protein-1, nitric oxide, superoxide, and hydrogen peroxide production in vitro by fluorometric detection. Also determined in vitro was serum-induced, monocyte adhesion and monocyte chemotactic activity. After 3 wk, significant reductions (P < 0.05) in body mass index, all serum lipids and lipid ratios, fasting glucose, insulin, homeostasis model assessment for insulin resistance, myeloperoxidase, 8-isoprostaglandin F2alpha, C-reactive protein, soluble ICAM-1, soluble P-selectin, macrophage inflammatory protein-1alpha, and matrix metalloproteinase-9 were noted. In vitro, serum-stimulated cellular VCAM-1 expression, monocyte chemotactic protein-1 production, and fluorometric detection of superoxide and hydrogen peroxide production decreased, whereas a concomitant increase in NO production was noted (all P < 0.01). Additionally, both monocyte adhesion (P < 0.05) and MCA (P < 0.01) decreased. Nine of 15 were no longer positive for metabolic syndrome postintervention. Intensive lifestyle modification may ameliorate novel coronary artery disease risk factors in men with metabolic syndrome factors before reversal of obesity. The present study was designed to examine the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress, inflammation, chemotaxis, and cell adhesion. Obese men (n = 31), 15 of whom had metabolic syndrome, were placed on a high-fiber, low-fat diet in a 3-wk residential program where food was provided ad libitum and daily aerobic exercise was performed. In each subject, pre- and postintervention fasting blood was drawn for circulating levels of serum lipids, glucose and insulin (for estimation of insulin sensitivity), oxidative stress-generating enzyme myeloperoxidase and marker 8-isoprostaglandin F sub(2 alpha ), the inflammatory protein C-reactive protein, soluble ICAM-1 as an indicator of endothelial activation, sP-selectin as a marker of platelet activation, the chemokine macrophage inflammatory protein-1 alpha , and total matrix metalloproteinase-9. Using subject sera and human aortic endothelial cell culture systems, we measured VCAM-1 cell surface abundance and monocyte chemotactic protein-1, nitric oxide, superoxide, and hydrogen peroxide production in vitro by fluorometric detection. Also determined in vitro was serum-induced, monocyte adhesion and monocyte chemotactic activity. After 3 wk, significant reductions (P < 0.05) in body mass index, all serum lipids and lipid ratios, fasting glucose, insulin, homeostasis model assessment for insulin resistance, myeloperoxidase, 8-isoprostaglandin F sub(2 alpha ), C-reactive protein, soluble ICAM-1, soluble P-selectin, macrophage inflammatory protein-1 alpha , and matrix metalloproteinase-9 were noted. In vitro, serum-stimulated cellular VCAM-1 expression, monocyte chemotactic protein-1 production, and fluorometric detection of superoxide and hydrogen peroxide production decreased, whereas a concomitant increase in NO production was noted (all P < 0.01). Additionally, both monocyte adhesion (P < 0.05) and MCA (P < 0.01) decreased. Nine of 15 were no longer positive for metabolic syndrome postintervention. Intensive lifestyle modification may ameliorate novel coronary artery disease risk factors in men with metabolic syndrome factors before reversal of obesity. |
Author | Won, Dean Roberts, Christian K Pruthi, Sandeep Vaziri, Nosratola D Kurtovic, Silvia Barnard, R. James Sindhu, Ram K |
Author_xml | – sequence: 1 fullname: Roberts, Christian K – sequence: 2 fullname: Won, Dean – sequence: 3 fullname: Pruthi, Sandeep – sequence: 4 fullname: Kurtovic, Silvia – sequence: 5 fullname: Sindhu, Ram K – sequence: 6 fullname: Vaziri, Nosratola D – sequence: 7 fullname: Barnard, R. James |
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Cites_doi | 10.1161/01.CIR.99.8.993 10.1161/01.ATV.14.11.1751 10.1080/00365510410006054 10.1210/jcem.85.7.6661 10.1161/hc0902.104353 10.1001/jama.1986.03380200073024 10.1074/jbc.M106958200 10.1172/JCI8574 10.1161/01.ATV.0000089012.73180.63 10.1093/clinchem/18.6.499 10.1097/00001648-200209000-00012 10.1016/S0022-2275(20)38461-3 10.1161/01.ATV.21.6.968 10.1001/jama.288.21.2709 10.1172/JCI115532 10.1080/003655102321004495 10.1002/jlb.60.6.692 10.1161/01.ATV.0000030997.02059.BB 10.1097/00041433-200208000-00003 10.1038/34923 10.1161/01.ATV.0000168573.10844.ae 10.1007/s00392-004-0146-5 10.1093/clinchem/47.3.444 10.1172/JCI117342 10.1056/NEJMoa012512 10.4159/harvard.9780674497887 10.1152/japplphysiol.00852.2004 10.1161/01.CIR.0000052617.91920.FD 10.1172/JCI118345 10.1001/jama.287.3.356 10.1161/01.ATV.17.11.2309 10.1161/01.CIR.92.2.197 10.1016/j.metabol.2003.10.016 10.1093/ajcn/53.5.1124 10.1001/archinte.1991.00400070141019 10.1056/NEJM200002173420702 10.1016/S0021-9150(99)00346-9 10.1056/NEJM200003233421202 10.1097/00005768-199905000-00004 10.1093/ajcn/75.3.492 10.1161/01.CIR.0000040584.91836.0D 10.1161/01.CIR.91.9.2488 10.1056/NEJMoa035003 10.1161/01.CIR.103.4.491 10.1016/S0014-5793(98)00440-2 10.1006/jmcc.1997.0497 10.1016/j.freeradbiomed.2004.06.003 10.1161/01.ATV.19.4.972 10.1093/oxfordjournals.aje.a116768 10.1074/jbc.M112400200 10.1001/jama.285.19.2486 10.1161/hc0702.104279 10.1006/abbi.1993.1222 10.1136/jim-51-05-17 10.2337/diacare.26.7.2119 |
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Snippet | 1 Department of Physiological Science, University of California, Los Angeles; 2 Division of Endocrinology, Metabolism and Molecular Medicine, Charles R. Drew... The present study was designed to examine the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress,... |
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SubjectTerms | Aged Biological and medical sciences Blood Glucose - analysis C-Reactive Protein - analysis C-Reactive Protein - physiology Cell Communication - physiology Cells, Cultured Chemokine CCL2 - metabolism Chemokine CCL2 - physiology Chemotaxis - physiology Endothelium, Vascular - pathology Endothelium, Vascular - physiopathology Feeding Behavior - physiology Fundamental and applied biological sciences. Psychology Humans Hydrogen Peroxide - metabolism Inflammation - physiopathology Insulin - blood Intercellular Adhesion Molecule-1 - blood Intercellular Adhesion Molecule-1 - physiology Lipids - blood Lipids - physiology Male Matrix Metalloproteinase 9 - blood Matrix Metalloproteinase 9 - physiology Metabolic Syndrome - blood Metabolic Syndrome - physiopathology Metabolic Syndrome - therapy Middle Aged Monocytes - pathology Monocytes - physiology Motor Activity - physiology Nitric Oxide - metabolism Nitric Oxide - physiology Obesity - blood Obesity - pathology Obesity - physiopathology Oxidative Stress - physiology P-Selectin - blood P-Selectin - physiology Superoxides - metabolism Vascular Cell Adhesion Molecule-1 - metabolism Vascular Cell Adhesion Molecule-1 - physiology |
Title | Effect of a short-term diet and exercise intervention on oxidative stress, inflammation, MMP-9, and monocyte chemotactic activity in men with metabolic syndrome factors |
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