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glutathione/adipositas
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Seite 1 von 1121 Ergebnisse
Glutathione-S-transferase M1, obesity, statins, and autonomic effects of particles: gene-by-drug-by-environment interaction.
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BACKGROUND
Air pollution by particulate matter (PM) has been associated with cardiovascular deaths, although the mechanism of action is unclear. One proposed pathway is through disturbances of the autonomic control of the heart.
OBJECTIVE
We tested the hypothesis that such disturbances are mediated
Lack of association between glutathione s-transferase mu 1 (GSTM1) gene polymorphisms and obesity.
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Recent researches suggested that personal individual's genetic background is contributed to the susceptibility to obesity. The present of this study is to investigate whether single nucleotide polymorphisms (SNPs) of glutathione s-transferase mu 1 (GSTM1) gene are susceptibility to obesity in Korean
High-fat-fed obese glutathione peroxidase 1-deficient mice exhibit defective insulin secretion but protection from hepatic steatosis and liver damage.
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OBJECTIVE
Reactive oxygen species (ROS) such as H2O2 can promote signaling through the inactivation of protein tyrosine phosphatases (PTPs). However, in obesity, the generation of ROS exceeds the antioxidant reserve and can contribute to the promotion of insulin resistance. Glutathione peroxidase 1
Glutathione S-transferase polymorphisms, passive smoking, obesity, and heart rate variability in nonsmokers.
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BACKGROUND
Disturbances of heart rate variability (HRV) may represent one pathway by which second-hand smoke (SHS) and air pollutants affect cardiovascular morbidity and mortality. The mechanisms are poorly understood.
OBJECTIVE
We investigated the hypothesis that oxidative stress alters cardiac
Insulin degradation. XVIII. On the regulation of glutathione-insulin transhydrogenase in the hyperglycemic obese (ob/ob) mouse.
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The occurrence of insulin-degrading activity in the liver of the obese hyperglycemic mouse (ob/ob) and its litter mate has been studied. The trichloroacetic acid-soluble product formed from insulin upon incubation with liver homogenate was identified as the A chain of insulin. In Ouchterlony
Monosodium glutamate-induced obesity changed the expression and activity of glutathione S-transferases in mouse heart and kidney.
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Obesity may affect activity and/or expression of enzymes participating in xenobiotics' detoxification and antioxidant defense. This study sought to investigate the activities and expression of cardiac and renal glutathione S-transferase (GST) isoforms in order to reveal possible differences between
Glutathione peroxidase activity in obese and nonobese diabetic patients and role of hyperglycemia in oxidative stress.
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BACKGROUND
Both hyperglycemia and obesity are known to cause oxidative stress, which leads to many complications associated with diabetes mellitus. A large number of diabetic patients are obese. Glutathione peroxidase (GPx) is an important indicator of level of oxidative stress.
METHODS
In the
Effect of obesity and troglitazone on expression of two glutathione peroxidases: cellular and extracellular types in serum, kidney and adipose tissue.
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To determine the effect of obesity on expression of cellular- (C-) and extracellular (EC-) glutathione peroxidase (GPX) in serum, kidney and adipose tissue, we measured GPX in serum, kidneys and adipose tissue of the obese Otsuka-Long-Evans-Tokushima Fatty (OLETF) rat and its lean counterpart
Glutathione S-transferase activity and isoenzyme concentrations in obese Avy/a and lean a/a mice.
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To assist in defining the mechanism(s) by which the activity of hepatic glutathione S-transferase (GST) is decreased in obese rodents, the cytosolic concentrations of individual GST isozymes were determined by high-performance liquid chromatography. For this purpose, liver cytosols from 8- and
Glutathione S-transferase (GST) polymorphism could be an early marker in the development of polycystic ovary syndrome (PCOS) - an insight from non-obese and non-insulin resistant adolescents.
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BACKGROUND
It has been supposed that endocrine disturbances might be responsible for polycystic ovary syndrome (PCOS)-associated oxida-tive stress, with special emphasis on hyperandrogenism. Considering the potential relationship between hyperandrogenism and increased free radical production,
Effect of hyperinsulinemia and type 2 diabetes-like hyperglycemia on expression of hepatic cytochrome p450 and glutathione s-transferase isoforms in a New Zealand obese-derived mouse backcross population.
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In subgroups of a New Zealand obese mouse-derived backcross population with defined aberrations of glucose homeostasis, a comprehensive study of the hepatic expression of cytochrome P450 and glutathione S-transferase was performed. Three patterns of alterations in response to insulin resistance
Hepatic glutathione S-transferase activity in mice: effects of Avy/-genotype, obesity, lindane treatment, and sex.
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Phenotypically distinct but genetically identical obese mottled yellow Avy/a and lean pseudoagouti Avy/a sibling mice and their congeneic black a/a littermates provide an experimental system for distinguishing phenotypic effects from genotypic effects in the expression of the genotype at the
A high-fat diet differentially regulates glutathione phenotypes in the obesity-prone mouse strains DBA/2J, C57BL/6J, and AKR/J.
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The ubiquitous tripeptide glutathione (GSH) is a critical component of the endogenous antioxidant defense system. Tissue GSH concentrations and redox status (GSH/GSSG) are genetically controlled, but it is unclear whether interactions between genetic background and diet affect GSH homeostasis. The
Glutathione levels in plasma, saliva and gingival crevicular fluid after periodontal therapy in obese and normal weight individuals.
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OBJECTIVE
The purpose of this study was to investigate the effects of obesity on reduced and oxidized glutathione (GSH and GSSG) levels in the gingival crevicular fluid, plasma and saliva of patients with chronic periodontitis and to evaluate the changes after nonsurgical periodontal
Parameters of metabolic syndrome and its relationship with zincemia and activities of superoxide dismutase and glutathione peroxidase in obese women.
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Alterations in antioxidant defense in obese people with metabolic syndrome can contribute to oxidative stress. This study assessed the relationship between the parameters of metabolic syndrome and the zincemia, activity of superoxide dismutase, and glutathione peroxidase enzymes in obese women.
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