Oxidative Stress in the Metabolic Syndrome

A great amount of scientific evidence supports that Oxidative Stress (OxS) can contribute to telomeric attrition and also plays an important role in the development of certain age-related diseases, among them the metabolic syndrome (MetS), which is characterised by clinical and biochemical alterations such as obesity, dyslipidaemia, arterial hypertension, hyperglycaemia, and insulin resistance, all of which are considered as risk factors for type 2 diabetes mellitus (T2DM) and cardiovascular diseases, which are associated in turn with an increase of OxS. In this sense, we review scientific evidence that supports the association between OxS with telomere length (TL) dynamics and the relationship with MetS components in aging. It was analysed whether each MetS component affects the telomere length separately or if they all affect it together. Likewise, this review provides a summary of the structure and function of telomeres and telomerase, the mechanisms of telomeric DNA repair, how telomere length may influence the fate of cells or be linked to inflammation and the development of age-related diseases, and finally, how the lifestyles can affect telomere length.

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Weight loss is associated with improved endothelial dysfunction via NOX2-generated oxidative stress down-regulation in patients with the metabolic syndrome

Internal and Emergency Medicine ◽

10.1007/s11739-011-0591-x ◽

2011 ◽

Vol 7 (3) ◽

pp. 219-227 ◽

Cited By ~ 31

Author(s):

Francesco Angelico ◽

Lorenzo Loffredo ◽

Pasquale Pignatelli ◽

Teresa Augelletti ◽

Roberto Carnevale ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Weight Loss ◽

Endothelial Dysfunction ◽

Down Regulation ◽

The Metabolic Syndrome

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Abstract 3672: Loss of Perivascular Adipocyte Paracrine Function Leads to Increased Vascular Tone and Glucose Intolerance in Hypertension

Circulation ◽

10.1161/circ.118.suppl_18.s_463-b ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Kaivan Khavandi ◽

Adam Greenstein ◽

Sarah Withers ◽

Kazuhiko Sonoyama ◽

Sarah Lewis ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Adipose Tissue ◽

Vascular Tone ◽

Tnf Alpha ◽

Perivascular Adipose Tissue ◽

The Metabolic Syndrome ◽

Adipocyte Cell ◽

Therapeutic Opportunity

In order to investigate the contribution of perivascular adipose tissue (PVAT) to arterial function, a total of 55 small arteries harvested from 35 skin biopsies of patients with Metabolic Syndrome and matched controls were mounted as ring preparations in a wire myograph. Contractility to cumulative doses of Norepinephrine in the presence or absence of PVAT showed an anticontractile effect in arteries from healthy volunteers (p=0.009), which was lost in patients with Metabolic Syndrome. Bioassay studies confirmed that PVAT releases a hydrophilic anticontractile factor in health, which is absent in obesity. Using a soluble fragment of the human Type 1 receptor, we identified that the anticontractile factor was adiponectin, which is the sole mediator of vasodilation, acting by increasing endothelial bioavailability of nitric oxide. Significant endothelial dysfunction was observed in patients with Metabolic Syndrome (p<0.001). Quantitative image analysis of adipose tissue revealed significantly increased adipocyte cell size in patients with Metabolic Syndrome, compared with healthy controls (p<0.006). There was immunohistochemical evidence of inflammation with upregulation of TNF-alpha receptor 1 in these patients (p<0.001). Application of exogenous TNF-alpha abolished the anticontractile effect of PVAT by reducing adiponectin bioavailability. Oxidative stress also induced by cytokines TNF-alpha and IL-6 but not IL-1, reduced adiponectin production from PVAT and increased basal tone. When the obese microenvironment was replicated in vitro by inflicting hypoxia on PVAT, adiponectin activity was lost but then rescued by incubation with cytokine antagonists. Further application of the adiponectin receptor fragment abolished PVAT relaxation. We conclude that in healthy arteries, PVAT releases adiponectin which reduces vascular tone. In obesity, this is lost by a cascade of adipocyte hypertrophy, hypoxia, inflammation and oxidative stress. The resulting vasoconstriction contributes to hypertension, hypertriglyceridaemia and insulin resistance. Direct targeting of adiponectin release from PVAT therefore provides a novel therapeutic opportunity in the Metabolic Syndrome.

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Exercise and diet induced weight loss improves measures of oxidative stress and insulin sensitivity in adults with characteristics of the metabolic syndrome

Yearbook of Sports Medicine ◽

10.1016/s0162-0908(08)79223-7 ◽

2008 ◽

Vol 2008 ◽

pp. 150-152

Author(s):

D.C. Nieman

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Weight Loss ◽

Insulin Sensitivity ◽

The Metabolic Syndrome

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Correlation of Ferritin and Transferrin Serum with hsCRP and F2-Isoprostane in Metabolic Syndrome

The Indonesian Biomedical Journal ◽

10.18585/inabj.v2i3.127 ◽

2010 ◽

Vol 2 (3) ◽

pp. 131

Author(s):

Waode Nurfina ◽

Irawan Yusuf ◽

Mansyur Arif

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Iron Status ◽

High Sensitivity ◽

C Reactive Protein ◽

Reactive Protein ◽

The Metabolic Syndrome ◽

Metabolic Conditions ◽

Inflammatory State ◽

And Oxidative Stress

BACKGROUND: The low inflammatory state that accompanies the Metabolic Syndrome (MetS) associates with the overexpression of oxidative stress. Ferritin and Transferrin serum are often used to measure iron status and their concentrations are altered in several metabolic conditions. We hypothesized that concentration of Ferritin and Transferrin serum increase in Metabolic Syndrome (MetS) and correlate with the inflammation and oxidative stress.METHODS: We studied 65 male MetS patients, aged 43.26±7.16 years. Iron metabolism was measured by concentration of Ferritin and Transferrin serums, while inflammatory and oxidative stress by high sensitivity C-reactive Protein (hsCRP) and F2-Isoprostane.RESULTS: Concentration of Ferritin 315.70±188.63 ng/L and Transferrin 2.36±0.31 g/L increased along with increasing components of MetS. Concentration of Ferritin serum had a positive correlation with hsCRP (r=0.220) and F2-Isoprostane (r=0.023).CONCLUSION: Serum concentration of Ferritin increased in the MetS and correlates with hsCRP and F2-Isoprostane.KEYWORDS: metabolic syndrome, ferritin, transferrin, hsCRP, F2-isoprostane

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Lipid Peroxidation as a Link Between Unhealthy Diets and the Metabolic Syndrome

10.5772/intechopen.98183 ◽

2021 ◽

Author(s):

Arnold N. Onyango

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Lipid Peroxidation ◽

Lipid Oxidation ◽

Saturated Fatty Acids ◽

Radical Scavenging ◽

The Metabolic Syndrome ◽

Mechanisms Of Formation ◽

Obesity Hypertension

Unhealthy diets, such as those high in saturated fat and sugar accelerate the development of non-communicable diseases. The metabolic syndrome is a conglomeration of disorders such as abdominal obesity, hypertension, impaired glucose regulation and dyslipidemia, which increases the risk for diabetes and cardiovascular disease. The prevalence of the metabolic syndrome is increasing globally, and dietary interventions may help to reverse this trend. A good understanding of its pathophysiological mechanisms is needed for the proper design of such interventions. This chapter discusses how lipid peroxidation is associated with the development of this syndrome, mainly through the formation of bioactive aldehydes, such as 4-hydroxy-2-nonenal, malondialdehyde, acrolein and glyoxal, which modify biomolecules to induce cellular dysfunction, including the enhancement of oxidative stress and inflammatory signaling. It gives a current understanding of the mechanisms of formation of these aldehydes and how dietary components such as saturated fatty acids promote oxidative stress, leading to lipid oxidation. It also outlines mechanisms, apart from free radical scavenging and singlet oxygen quenching, by which various dietary constituents prevent oxidative stress and lipid oxidation in vivo.

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Effect ofBifidobacterium lactisHN019 on inflammatory markers and oxidative stress in subjects with and without the metabolic syndrome

British Journal Of Nutrition ◽

10.1017/s0007114518001861 ◽

2018 ◽

Vol 120 (6) ◽

pp. 645-652 ◽

Cited By ~ 5

Author(s):

Luciana J. Bernini ◽

Andréa N. Colado Simão ◽

Cínthia H. B. de Souza ◽

Daniela F. Alfieri ◽

Liliane G. Segura ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Inflammatory Markers ◽

Healthy Subjects ◽

Antioxidant Defenses ◽

Beneficial Effects ◽

The Metabolic Syndrome ◽

Inflammatory State ◽

Baseline Values ◽

And Oxidative Stress

AbstractBeneficial effects of probiotics have been reported on body weight, lipid and carbohydrate metabolism, inflammatory state and oxidative stress in healthy subjects and in many metabolic and inflammatory diseases. The aim of this study was to evaluate the effects ofBifidobacterium lactisHN019 on inflammatory state and nitro-oxidative stress in patients with and without the metabolic syndrome (MetS). The usual diets of the thirty-three subjects were supplemented with probiotic milk for 90 d. Inflammatory markers and oxidative measurements were performed. In relation to the baseline values, subjects in both groups showed a decrease in homocysteine (P=0·02 andP=0·03, respectively), hydroperoxides (P=0·02 andP=0·01, respectively) and IL-6 levels (P=0·02). Increases in adiponectin (P=0·04) and nitric oxide metabolites (NOx,P=0·001) levels were only seen in the group with the MetS in relation to the baseline values, whereas only the individuals without the MetS had increases in total radical-trapping antioxidant parameter levels (P=0·002). In conclusion,B. lactisHN019 have several beneficial effects on inflammatory and oxidative biomarkers in healthy subjects and the MetS patients. Patients with the MetS showed a specific improvement in adiponectin and NOx levels, whereas a specific favourable effect was shown in the antioxidant defenses in healthy subjects. If the results obtained in the present study are confirmed, supplementation of fermented milk with probiotics in healthy subjects and patients with the MetS must be further discussed.

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Abstract 1125: Mulberry Leaf Ameliorates The Production Of Adipocytokines By Inhibiting Oxidative Stress In White Adipose Tissue In db/db Mice

Circulation ◽

10.1161/circ.116.suppl_16.ii_226-c ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Masayuki Sugimoto ◽

Hidenori Arai ◽

Yukinori Tamura ◽

Toshinori Murayama ◽

Koh Ono ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Adipose Tissue ◽

White Adipose Tissue ◽

Metabolic Disorders ◽

The Body ◽

Mulberry Leaf ◽

The Metabolic Syndrome ◽

Pparγ Agonist ◽

Tnf Α

Mulberry leaf (ML) is commonly used to feed silkworms. Previous study showed that ML ameliorates atherosclerosis. However, its mechanism is not completely understood. Because dysregulated production of adipocytokines is involved in the development of the metabolic syndrome and cardiovascular disease, we examined the effect of ML on the production of adipocytokines and metabolic disorders related to the metabolic syndrome, and compared its effect with that of a PPARγ agonist, pioglitazone (Pio). By treating obese diabetic db/db mice with ML, Pio, and their combination, we investigated the mechanism by which they improve metabolic disorders. In this study, db/+m (lean control) and db/db mice were fed a standard diet with or without 3% (w/w) ML and/or 0.01% (w/w) Pio for 12 weeks from 9 weeks of age. At the end of the experiment we found that ML decreased plasma glucose and triglyceride by 32% and 30%, respectively. Interestingly, administration of ML in addition to Pio showed additive effects; further 40% and 30% reduction in glucose and triglyceride compared with Pio treatment, respectively. Moreover, administration of ML in addition to Pio suppressed the body weight increase by Pio treatment and reduced visceral/subcutaneous fat ratio by 20% compared with control db/db mice. Importantly, ML treatment increased expression of adiponectin in white adipose tissue (WAT) by 40%, which was only found in db/db mice, not in control db/+m mice. Combination of ML and Pio increased plasma adiponectin concentrations by 25% and its expression in WAT by 17% compared with Pio alone. In contrast, ML decreased expression of TNF-α and MCP-1 by 25% and 20%, respectively, and the addition of Pio resulted in a further decrease of these cytokines by about 45%. To study the mechanism, we examined the role of oxidative stress. ML decreased the amount of lipid peroxides by 43% and the expression of NADPH oxidase subunits in WAT, which was consistent with the results of TNF-α and MCP-1. Thus our results indicate that ML ameliorates adipocytokine dysregulation by inhibiting oxidative stress in WAT of obese mice, and that ML may have a potential for the treatment of the metabolic syndrome as well as reducing adverse effects of Pio.

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The Niemann-Pick C1 Like 1 (NPC1L1) Inhibitor Ezetimibe Improves Metabolic Disease Via Decreased Liver X Receptor (LXR) Activity in Liver of Obese Male Mice

Endocrinology ◽

10.1210/en.2013-2143 ◽

2014 ◽

Vol 155 (8) ◽

pp. 2810-2819 ◽

Cited By ~ 20

Author(s):

Taichi Sugizaki ◽

Mitsuhiro Watanabe ◽

Yasushi Horai ◽

Nao Kaneko-Iwasaki ◽

Eri Arita ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Insulin Signaling ◽

Metabolic Diseases ◽

In Vitro Study ◽

Liver X Receptor ◽

Gene Expressions ◽

The Metabolic Syndrome ◽

Increased Risk

Dyslipidemic patients with diabetes mellitus, including metabolic syndrome, are at increased risk of coronary heart disease. It has been reported that ezetimibe, a cholesterol absorption inhibitor, improves metabolic diseases in mice and humans. However, the underlying mechanism has been unclear. Here we explored the effects of ezetimibe on lipid and glucose homeostasis. Male KK-Ay mice were fed a high-fat diet, which is the mouse model of metabolic syndrome, with or without ezetimibe for 14 weeks. Ezetimibe improved dyslipidemia, steatosis, and insulin resistance. Ezetimibe decreased hepatic oxysterols, which are endogenous agonists of liver X receptor (LXR), to decrease hepatic lipogenic gene expressions, especially in stearoyl-CoA desaturase-1 (SCD1), leading to a remarkable reduction of hepatic oleate content that would contribute to the improvement of steatosis by reducing triglycerides and cholesterol esters. Simultaneously, hepatic β-oxidation, NADPH oxidase and cytochrome P450 2E1 (CYP2E1) were reduced, and thus reactive oxygen species (ROS) and inflammatory cytokines were also decreased. Consistent with these changes, ezetimibe diminished c-Jun N-terminal kinase (JNK) phosphorylation and improved insulin signaling in the liver. In vitro study using primary hepatocytes obtained from male SD rats, treated with oleate and LXR agonist, showed excess lipid accumulation, increased oxidative stress and impaired insulin signaling. Therefore, in obese subjects, ezetimibe reduces hepatic LXR activity by reducing hepatic oxysterols to lower hepatic oleate content. This improves steatosis and reduces oxidative stress, and this reduction improves insulin signaling in the liver. These results provide insight into pathogenesis and strategies for treatment of the metabolic syndrome.

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