Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with metabolic syndrome show augmented cardio-vascular risk, at least in part mediated through disequilibrium between mechanisms generating free radicals, and antioxidant defense. Carbohydrate and lipid disturbances in metabolic syndrome induce oxidative stress via several non fully understood mechanisms. Glucose overload in oral glucose tolerance test (OGTT) can also induce oxidative stress. The aim of our study was to evaluate changes in superoxide dismutase and glutathione peroxidase activity, as well as total antioxidant status in OGTT in patients with metabolic syndrome and in healthy subjects. OGTT was performed in 36 healthy volunteers and in patients with metabolic syndrome. Glucose, Insulin, and triglycerides were evaluated at 0th, 30th, 60th, 120th, and 180th min. Superoxide dismutase and glutathione peroxidase were measured at 0th, 60th, and 120th min. Total antioxidant status was measured at 0th, and 120th min. At 0th min total, HDL and LDL cholesterol were evaluated. A statistically significant decrease (p < 0.05) in superoxide dismutase activity at 120th as compared with 60th min were observed. Glutathione peroxidase activity decreased significantly (p < 0.05) even though at 60th as compared with 0th min and remained decreased at 120th min. Total antioxidant status was found to be increased (p < 0.05) at 120th as compared with 0th min. The observed dynamic in patients did not differed (p > 0.05) from control group. The study shows a decrease in antioxidant enzyme activity and a compensatory increase in total antioxidant status, indicating a surcharge of antioxidant homeostasis. In context of carbohydrate and lipid disturbances in metabolic syndrome, this is to suggest an existing of complementary pathogenic mechanisms, able to aggravate cardiovascular risk in these patients. Correction of metabolic disturbances may be an efficacious tool for influencing on prooxidant-antioxidant homeostasis too.
 ...
PMID:[Antioxidant parameters in metabolic syndrome -- a dynamic evaluation during oral glucose tolerance test]. 1200 76

The aim of this study was to investigate the association between metabolic syndrome (MetS) and the metabolic indicators of masticatory muscles in an animal model. A total of 16 male Wistar rats were used. To induce MetS, 10 rats were fed with standard rat chow and 32% sucrose solution ad libitum for 16 wk. Six rats fed with standard rat chow and water ad libitum formed the control group. All rats were killed at week 16, and the right superficial masseter muscles were harvested. Metabolic indicators of masticatory muscle metabolism, including antioxidant enzyme activities, ion transport ATPase activities, and the levels of macro and trace elements, were determined in the muscles. Superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities were significantly decreased by 32%, 26%, 33%, and 16%, respectively, in the MetS group. Na(+) /K(+) -ATPase activity was significantly decreased in the MetS group by 54% compared with the control group. The levels of chromium and selenium were significantly decreased, and the level of copper was increased, in the MetS group compared with the control group. These results show that significant alterations occurred in antioxidant defense mechanisms, ion transport mechanisms, and trace element levels of masseter muscles in MetS.
...
PMID:Effects of metabolic syndrome on masseter muscle of male Wistar rats. 2652 68

Reactive oxygen species (ROS) are key mediators of several cellular damage and thus associated with equine diseases such as inflammation and metabolic syndrome. This study aimed to evaluate the protective and antioxidant activities of methanolic extract prepared from Cladophora glomerata (C. glomerata) biomass, on equine adipose derived mesenchymal stem cells (EqASCs), under experimental oxidative stress induced by H2O2. Pre-treatment of EqASCs cells with different concentrations of C. glomerata methanolic extract (1% and 5%) provided a clear protection against cellular damage triggered by H2O2. The cell's apoptotic status was significantly regulated, with promotion of cell viability, down-regulation of pro-apoptotic (p21, p53, Bax and Casp-9) genes expression, concomitant to up-regulation of the survival gene Bcl-2, this being supported by a mitigation of the endoplasmic reticulum (ER) stress and significant minimization of mitochondrial dysfunction. The results also showed that C. glomerata extract significantly increased the antioxidant enzymes Superoxide dismutase (SOD) and Catalase (CAT) activities, positively regulated the enzymes genes expression, and markedly reduced the protein carbonyls derivatives production. Finally, RT-qPCR analysis of the inflammatory related genes allowed to highlight a promising anti-inflammatory and immunomodulatory effect of this extract. Due to the valuable antioxidant and anti-inflammatory activities, C. glomerata may have potential benefits for the prevention of equine diseases associated with oxidative stress, including metabolic syndrome.
 ...
PMID:Cladophora glomerata methanolic extract decreases oxidative stress and improves viability and mitochondrial potential in equine adipose derived mesenchymal stem cells (ASCs). 3055 32

This is the first study to evaluate both the antioxidant barrier, glutathione metabolism, and oxidative damage to proteins and lipids in morbidly obese patients undergoing bariatric treatment. The study included 65 patients with class 3 obesity divided into two subgroups: morbidly obese patients without metabolic syndrome (OB) and obese patients with metabolic syndrome (OB + MS). Blood samples were collected before surgery as well as one, three, six, and twelve months after the bariatric treatment. Superoxide dismutase and reduced glutathione (GSH) were significantly decreased, whereas glutathione reductase and uric acid were enhanced in morbidly obese patients before bariatric surgery as compared to lean control. Moreover, in the OB group, we observed the increase of superoxide dismutase (SOD) and the decrease of uric acid (UA) after the bariatric treatment; however, these changes were not observed in the OB + MS group. The oxidative damage to proteins (advanced glycation end products, AGE; advanced oxidation protein products, AOPP) and lipids (8-isoprostanes, 8-isop; 4-hydroxynoneal) was higher in OB as well as OB + MS patients. We noticed that AGE and AOPP levels diminished after the bariatric treatment, whereas redox status (ratio of GSH to oxidized glutathione) was still reduced in the OB + MS group. Summarizing, morbid obesity is associated with disturbances in the antioxidant barrier and enhanced oxidative damage to proteins and lipids. Although bariatric surgery improves redox homeostasis in obese patients, those with metabolic syndrome show a continuous decrease in the antioxidant status. In patients undergoing bariatric treatment, antioxidant supplementation may be considered.
 ...
PMID:A Longitudinal Study of the Antioxidant Barrier and Oxidative Stress in Morbidly Obese Patients after Bariatric Surgery. Does the Metabolic Syndrome Affect the Redox Homeostasis of Obese People? 3224 12