Effect of Zinc Supplementation on Markers of Insulin Resistance, Oxidative Stress, and Inflammation among Prepubescent Children with Metabolic Syndrome

2010 ◽  
Vol 8 (6) ◽  
pp. 505-510 ◽  
Author(s):  
Roya Kelishadi ◽  
Mahin Hashemipour ◽  
Khosrow Adeli ◽  
Naser Tavakoli ◽  
Ahmad Movahedian-Attar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Zinc Supplementation

Oxidative stress and metabolic syndrome: Effects of a natural antioxidants enriched diet on insulin resistance

2015 ◽  
Vol 10 (2) ◽  
pp. e52-e60 ◽  
Author(s):  
Antonio Mancini ◽  
Giuseppe Ettore Martorana ◽  
Marinella Magini ◽  
Roberto Festa ◽  
Sebastiano Raimondo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Natural Antioxidants

Homocysteine is the confounding factor of metabolic syndrome-confirmed by siMS score

2018 ◽  
Vol 33 (2) ◽  
pp. 99-103 ◽  
Author(s):  
Branko Srećković ◽  
Ivan Soldatovic ◽  
Emina Colak ◽  
Igor Mrdovic ◽  
Mirjana Sumarac-Dumanovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Risk Score ◽  
Continuous Measure ◽  
Model Assessment ◽  
Anthropometric Parameters ◽  
Apo B ◽  
Significant Difference ◽  
Homeostatic Model Assessment

Abstract Background: Abdominal adiposity has a central role in developing insulin resistance (IR) by releasing pro-inflammatory cytokines. Patients with metabolic syndrome (MS) have higher values of homocysteine. Hyperhomocysteinemia correlates with IR, increasing the oxidative stress. Oxidative stress causes endothelial dysfunction, hypertension and atherosclerosis. The objective of the study was to examine the correlation of homocysteine with siMS score and siMS risk score and with other MS co-founding factors. Methods: The study included 69 obese individuals (age over 30, body mass index [BMI] >25 kg/m2), classified into two groups: I-with MS (33 patients); II-without MS (36 patients). Measurements included: anthropometric parameters, lipids, glucose regulation parameters and inflammation parameters. IR was determined by homeostatic model assessment for insulin resistance (HOMA-IR). ATP III classification was applied for diagnosing MS. SiMS score was used as continuous measure of metabolic syndrome. Results: A significant difference between groups was found for C-reactive protein (CRP) (p<0.01) apolipoprotein (Apo) B, HOMA-IR and acidum uricum (p<0.05). siMS risk score showed a positive correlation with homocysteine (p=0.023), while siMS score correlated positively with fibrinogen (p=0.013), CRP and acidum uricum (p=0.000) and homocysteine (p=0.08). Homocysteine correlated positively with ApoB (p=0.036), HbA1c (p=0.047), HOMA-IR (p=0.008) and negatively with ApoE (p=0.042). Conclusions: Correlation of siMS score with homocysteine, fibrinogen, CRP and acidum uricum indicates that they are co-founding factors of MS. siMS risk score correlation with homocysteine indicates that hyperhomocysteinemia increases with age. Hyperhomocysteinemia is linked with genetic factors and family nutritional scheme, increasing the risk for atherosclerosis.

scholarly journals Galantamine alleviates oxidative stress alongside anti-inflammatory and cardio-metabolic effects in subjects with the metabolic syndrome in a randomized trial

2020 ◽  
Author(s):  
Carine Teles Sangaleti ◽  
Keyla Yukari Katayama ◽  
Kátia De Angelis ◽  
Tércio Lemos de Moraes ◽  
Amanda Aparecida Araújo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Autonomic Regulation ◽  
Metabolic Effects ◽  
Antioxidant Enzyme Activities ◽  
Low Grade ◽  
The Metabolic Syndrome ◽  
Inflammatory State ◽  
Anti Inflammatory

AbstractBackgroundThe metabolic syndrome (MetS) is an obesity-driven disorder with pandemic proportions and limited treatment options. Oxidative stress, low-grade inflammation and altered autonomic regulation, are important components of MetS pathophysiology. We recently reported that galantamine, an acetylcholinesterase inhibitor and an FDA-approved drug (for Alzheimer’s disease) alleviates the inflammatory state in MetS subjects. Here we examined the effects of galantamine on oxidative stress in parallel with inflammatory and cardio-metabolic parameters in subjects with MetS.MethodsThe effects of galantamine treatment, 8 mg daily for 4 weeks, followed by 16 mg daily for 8 weeks or placebo were studied in randomly assigned subjects with MetS (n=22 per group) of both genders. Oxidative stress, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase activities, lipid and protein peroxidation, and nitrite levels were analyzed before and at the end of the treatment. In addition, plasma cytokine and adipokine levels, insulin resistance (HOMA-IR) and other relevant cardio-metabolic indices were analyzed. Autonomic regulation was also examined by heart rate variability (HRV) before treatment, and at every 4 weeks of treatment.ResultsGalantamine treatment significantly increased antioxidant enzyme activities, including SOD (+1.65 USOD/mg protein, [95% CI 0.39 to 2.92], P=0.004) and CAT (+0.93 nmol/mg, [95% CI 0.34 to 1.51], P=0.011), decreased lipid peroxidation (thiobarbituric acid reactive substances, -5.45 pmol/mg, [95% CI -10.97 to 0.067], P=0.053) and systemic nitrite levels (-0.05 nit/mg protein, [95% CI -0.21 to 0.10], P=0.038) compared with placebo. In addition, galantamine significantly alleviated the inflammatory state and insulin resistance, and decreased the low frequency/high frequency ratio of HRV, following 8 and 12 weeks of drug treatment.ConclusionLow-dose galantamine alleviates oxidative stress, alongside beneficial anti-inflammatory, and metabolic effects, and modulates autonomic regulation in subjects with MetS. These findings are of considerable interest for further studies with galantamine to ameliorate MetS pathophysiology.

Preventive Effect of Different Wild Pistachio Oils on Oxidative Stress Markers, Liver Enzymes, and Histopathological Findings in a Metabolic Syndrome Model

2019 ◽  
Vol 8 ◽  
pp. 1238
Author(s):  
Sanaz Jamshidi ◽  
Najmeh Hejazi ◽  
Mohammad-Taghi Golmakani ◽  
Nader Tanideh ◽  
Mina Heidari Esfahani
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Normal Saline ◽  
Liver Enzymes ◽  
Therapeutic Effects ◽  
Oxidative Stress Markers ◽  
Histopathological Findings ◽  
Kernel Oil ◽  
Stress Markers

Background: Wild pistachio (Pistacia Atlantica mutica) species with wide distribution in Iran have different nutrition properties and may have therapeutic effects in metabolic syndrome. Metabolic syndrome, as a prevalent health problem, is a main risk factor for different chronic diseases such as diabetes, fatty liver and cardiovascular diseases. The present study aimed to evaluate the preventive effects of mixture, kernel, and hull oil of wild pistachio (WP) on oxidative stress markers, liver function and histopathological findings in metabolic syndrome induced rats. Materials and Methods: After oil extraction by cold press method and chemical analysis, rats were divided into 6 groups. Group 1 received normal saline;  group 2 received 2cc fructose solution and 0.5cc normal saline; and groups 3, 4, 5 and 6 received 2 cc fructose solution and 0.5 cc sunflower oil, mixture, hull and kernel oils of WP for 10 weeks, respectively. Then, glycemic indices, oxidative stress, liver enzymes and histopathological examination were determined using standard laboratory tests. Results: WP Kernel and mixture oils notably decreased the fasting blood sugar and insulin resistance compared with the fructose group. Insulin level was significantly increased in the kernel oil group (P<0.05). There was no significant difference in oxidative stress, liver enzymes and histopathology parameters among the groups. Conclusion: Kernel oil of WP improved hyperglycemia, insulin resistance and insulin secretion, but the changes in oxidative stress markers, liver enzymes and histopathologic results were not significant among the groups. [GMJ.2019;In press:e1238]

scholarly journals Angiotensin receptor-mediated oxidative stress is associated with impaired cardiac redox signaling and mitochondrial function in insulin-resistant rats

2013 ◽  
Vol 305 (4) ◽  
pp. H599-H607 ◽  
Author(s):  
José Pablo Vázquez-Medina ◽  
Irina Popovich ◽  
Max A. Thorwald ◽  
Jose A. Viscarra ◽  
Ruben Rodriguez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Protein Expression ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Cellular Metabolism ◽  
Redox Signaling ◽  
Angiotensin Receptor ◽  
Long Evans

Activation of angiotensin receptor type 1 (AT1) contributes to NADPH oxidase (Nox)-derived oxidative stress during metabolic syndrome. However, the specific role of AT1 in modulating redox signaling, mitochondrial function, and oxidative stress in the heart remains more elusive. To test the hypothesis that AT1 activation increases oxidative stress while impairing redox signaling and mitochondrial function in the heart during diet-induced insulin resistance in obese animals, Otsuka Long Evans Tokushima Fatty (OLETF) rats ( n = 8/group) were treated with the AT1 blocker (ARB) olmesartan for 6 wk. Cardiac Nox2 protein expression increased 40% in OLETF compared with age-matched, lean, strain-control Long Evans Tokushima Otsuka (LETO) rats, while mRNA and protein expression of the H2O2-producing Nox4 increased 40–100%. ARB treatment prevented the increase in Nox2 without altering Nox4. ARB treatment also normalized the increased levels of protein and lipid oxidation (nitrotyrosine, 4-hydroxynonenal) and increased the redox-sensitive transcription factor Nrf2 by 30% and the activity of antioxidant enzymes (SOD, catalase, GPx) by 50–70%. Citrate synthase (CS) and succinate dehydrogenase (SDH) activities decreased 60–70%, whereas cardiac succinate levels decreased 35% in OLETF compared with LETO, suggesting that mitochondrial function in the heart is impaired during obesity-induced insulin resistance. ARB treatment normalized CS and SDH activities, as well as succinate levels, while increasing AMPK and normalizing Akt, suggesting that AT1 activation also impairs cellular metabolism in the diabetic heart. These data suggest that the cardiovascular complications associated with metabolic syndrome may result from AT1 receptor-mediated Nox2 activation leading to impaired redox signaling, mitochondrial activity, and dysregulation of cellular metabolism in the heart.

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