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      Lipid Peroxidation, Nitric Oxide Metabolites, and Their Ratio in a Group of Subjects with Metabolic Syndrome

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          Abstract

          Our aim was to evaluate lipid peroxidation, expressed as thiobarbituric acid-reactive substances (TBARS), nitric oxide metabolites (nitrite + nitrate) expressed as NO x , and TBARS/NO x ratio in a group of subjects with metabolic syndrome (MS). In this regard we enrolled 106 subjects with MS defined according to the IDF criteria, subsequently subdivided into diabetic (DMS) and nondiabetic (NDMS) and also into subjects with a low triglycerides/HDL-cholesterol (TG/HDL-C) index or with a high TG/HDL-C index. In the entire group and in the four subgroups of MS subjects we found an increase in TBARS and NO x levels and a decrease in TBARS/NO x ratio in comparison with normal controls. Regarding all these parameters no statistical difference between DMS and NDMS was evident, but a significant increase in NO x was present in subjects with a high TG/HDL-C index in comparison with those with a low index. In MS subjects we also found a negative correlation between TBARS/NO x ratio and TG/HDL-C index. Considering the hyperactivity of the inducible NO synthase in MS, these data confirm the altered redox and inflammatory status that characterizes the MS and suggest a link between lipid peroxidation, inflammation, and insulin resistance, evaluated as TG/HDL-C index.

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          Relationship between insulin resistance and an endogenous nitric oxide synthase inhibitor.

          Increased levels of asymmetric dimethylarginine (ADMA) are associated with endothelial dysfunction and increased risk of cardiovascular disease. Several cardiovascular risk factors are associated with reduced sensitivity to insulin, but elevated ADMA concentrations have not been fully linked to the metabolic syndrome. To evaluate the relationship between insulin sensitivity and plasma ADMA concentrations, and to determine whether a pharmacological treatment that increases insulin sensitivity would also modulate ADMA concentrations. Cross-sectional study, containing a nonrandomized controlled trial component, of 64 healthy volunteers without diabetes (42 women, 22 men; 48 with normal blood pressure and 16 with hypertension), which was conducted at a university medical center between October 2000 and July 2001. Rosiglitazone (4 mg/d for 4 weeks and then 4 mg twice daily for 8 weeks), an insulin-sensitizing agent, was given to 7 insulin-resistant subjects with hypertension. These subjects were studied before and after 12-week treatment. Insulin sensitivity measured by the insulin suppression test, and fasting plasma levels of low-density lipoprotein cholesterol, triglycerides, high-density lipoprotein cholesterol, glucose, insulin, and ADMA concentrations. Plasma ADMA concentrations were positively correlated with impairment of insulin-mediated glucose disposal in nondiabetic, normotensive subjects (r = 0.73; P<.001). Consistent with the metabolic syndrome, ADMA levels were also positively correlated with fasting triglyceride levels (r = 0.52; P<.001) but not with low-density lipoprotein cholesterol levels (r = 0.19; P =.20). Plasma ADMA concentrations increased in insulin-resistant subjects independent of hypertension. Pharmacological treatment improved insulin sensitivity and reduced mean (SD) plasma ADMA concentrations from 1.50 (0.30) to 1.05 (0.33) micromol/L (P =.001). A significant relationship exists between insulin resistance and plasma concentrations of ADMA. Pharmacological intervention with rosiglitazone enhanced insulin sensitivity and reduced ADMA levels. Increases in plasma ADMA concentrations may contribute to the endothelial dysfunction observed in insulin-resistant patients.
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            Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the metabolic syndrome, and associated vascular and neurodegenerative disorders.

            A rising tide of obesity and type 2 diabetes has resulted from the development of technologies that have made inexpensive high calorie foods readily available and exercise unnecessary for many people. Obesity and the metabolic syndrome (insulin resistance, visceral adiposity and dyslipidemia) wreak havoc on cells throughout the body thereby promoting cardiovascular and kidney disease, and degenerative diseases of the brain and body. Obesity and insulin resistance promote disease by increasing oxidative damage to proteins, lipids and DNA as the result of a combination of increased free radical production and an impaired ability of cells to detoxify the radicals and repair damaged molecules. By covalently modifying membrane-associated proteins, the membrane lipid peroxidation product 4-hydroxynonenal (HNE) may play particularly sinister roles in the metabolic syndrome and associated disease processes. HNE can damage pancreatic beta cells and can impair the ability of muscle and liver cells to respond to insulin. HNE may promote atherosclerosis by modifying lipoproteins and can cause cardiac cell damage by impairing metabolic enzymes. An adverse role for HNE in the brain in obesity and the metabolic syndrome is suggested by studies showing that HNE levels are increased in brain cells with aging and Alzheimer's disease. HNE can cause the dysfunction and degeneration of neurons by modifying membrane-associated glucose and glutamate transporters, ion-motive ATPases, enzymes involved in amyloid metabolism, and cytoskeletal proteins. Exercise and dietary energy restriction reduce HNE production and may also increase cellular systems for HNE detoxification including glutathione and oxidoreductases. The recent development of low molecular weight molecules that scavenge HNE suggests that HNE can be targeted in the design of drugs for the treatment of obesity, the metabolic syndrome, and associated disorders.
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              Malondialdehyde (MDA) and protein carbonyl (PCO) levels as biomarkers of oxidative stress in subjects with familial hypercholesterolemia.

              Familial hypercholesterolemia (FH) is clinically characterized by elevated total and low-density lipoprotein (LDL) cholesterol levels in plasma, which has high risk for developing atherosclerosis. Increased oxidative stress (OS) and FH have been related to atherosclerosis. The study aims to evaluate oxidative stress in patients with hypercholesterolemia by measuring lipid peroxidation and protein carbonyl (PCO) levels in these patients. PCO in these patients may provide a new diagnostic biomarker for oxidative damage in atherosclerosis. Total cholesterol (Tc), low-density lipoprotein-cholesterol (LDL-c), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-c), lipoprotein(a) (Lp-a) levels and carotid intima-media thickness were measured to evaluate characteristics of patients (11 homozygous and 25 heterozygous) with FH. 25 age-gender-BMI matched healthy control subjects were included in the study for comparison. MDA and PCO levels were significantly higher in homozygous patients compared with those of heterozygous and controls and it was found that they are positively correlated with LDL-c, Tc, Lp-a and IMT while negatively correlated with HDL-c. The heterozygous group also had significantly higher MDA and PCO levels compared with controls. The data obtained could be important for understanding the alterations presented by FH and could be related to their increased risk of developing atherosclerosis. To our knowledge, measurements of PCO in patients with FH are not recorded before and this may be used as a biomarker for protein oxidation, which may play a role in the increased cardiovascular risk of patients with FH. Copyright © 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Oxid Med Cell Longev
                Oxid Med Cell Longev
                OMCL
                Oxidative Medicine and Cellular Longevity
                Hindawi Publishing Corporation
                1942-0900
                1942-0994
                2014
                2 June 2014
                : 2014
                : 824756
                Affiliations
                Dipartimento Biomedico di Medicina Interna e Specialistica, Università di Palermo, Via del Vespro 129, 90100 Palermo, Italy
                Author notes

                Academic Editor: Vladimir Jakovljevic

                Author information
                http://orcid.org/0000-0002-5346-2829
                http://orcid.org/0000-0001-5175-5727
                Article
                10.1155/2014/824756
                4060162
                d4a8fe89-b4a7-4a50-bfdc-56efe9128b6a
                Copyright © 2014 Gregorio Caimi et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 31 March 2014
                : 13 May 2014
                : 17 May 2014
                Categories
                Research Article

                Molecular medicine
                Molecular medicine

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