A role for glutathione peroxidase in protecting pancreatic beta cells against oxidative stress in a model of glucose toxicity. - Wikidata - awgldk - TriplyDB

A role for glutathione peroxidase in protecting pancreatic beta cells against oxidative stress in a model of glucose toxicity.

A role for glutathione peroxidase in protecting pancreatic beta cells against oxidative stress in a model of glucose toxicity.

http://www.wikidata.org/entity/Q34156113

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Selenium and Metabolic Disorders: An Emphasis on Type 2 Diabetes Risk Molecular Events Linking Oxidative Stress and Inflammation to Insulin Resistance and β-Cell Dysfunction Metabolomics applied to the pancreatic islet Natural history of β-cell adaptation and failure in type 2 diabetes Obesity, Oxidative Stress, Adipose Tissue Dysfunction, and the Associated Health Risks: Causes and Therapeutic Strategies Adenoviral overexpression of the glutamylcysteine ligase catalytic subunit protects pancreatic islets against oxidative stress Chemical methods for the simultaneous quantitation of metabolites and proteins from single cells The antioxidant N-Acetylcysteine does not improve glucose tolerance or β-cell function in type 2 diabetes.Early low protein diet aggravates unbalance between antioxidant enzymes leading to islet dysfunction.Diabetic beta-cells can achieve self-protection against oxidative stress through an adaptive up-regulation of their antioxidant defenses.ATP-sensitive K+ channel mediates the zinc switch-off signal for glucagon response during glucose deprivation.An islet in distress: β cell failure in type 2 diabetes.Antioxidant enzymes and lipid peroxidation in endometrium of patients with polyps, myoma, hyperplasia and adenocarcinoma.Glucose induces pancreatic islet cell apoptosis that requires the BH3-only proteins Bim and Puma and multi-BH domain protein Bax.Thresholds of oxidative stress in newly diagnosed diabetic patients on intensive glucose-control therapy.High glucose inhibits glucose-6-phosphate dehydrogenase, leading to increased oxidative stress and beta-cell apoptosis.The role of oxidative stress in the pathogenesis of type 2 diabetes: from molecular mechanism to clinical implication.Heterozygous SOD2 deletion impairs glucose-stimulated insulin secretion, but not insulin action, in high-fat-fed mice.Impacts of dietary selenium deficiency on metabolic phenotypes of diet-restricted GPX1-overexpressing mice Two tales of antioxidant enzymes on β cells and diabetes.Knockouts of SOD1 and GPX1 exert different impacts on murine islet function and pancreatic integrity mtDNA G10398A variation provides risk to type 2 diabetes in population group from the Jammu region of India.Nigella sativa improves glycemic control and ameliorates oxidative stress in patients with type 2 diabetes mellitus: placebo controlled participant blinded clinical trial.Proteasome dysfunction mediates high glucose-induced apoptosis in rodent beta cells and human islets Type 2 diabetes and the aging pancreatic beta cell.Activation of the NLRP3 inflammasome complex is not required for stress-induced death of pancreatic islets.Protective Effect of Heme Oxygenase-1 on High Glucose-Induced Pancreatic β-Cell Injury.Glucose-Dependent Insulin Secretion in Pancreatic β-Cell Islets from Male Rats Requires Ca2+ Release via ROS-Stimulated Ryanodine Receptors.Gliclazide does not fully prevent 2-deoxy-D-ribose-induced oxidative damage because it does not restore glutathione content in a pancreatic β-cell line.A simple matter of life and death-the trials of postnatal Beta-cell mass regulation A Syntenic Cross Species Aneuploidy Genetic Screen Links RCAN1 Expression to β-Cell Mitochondrial Dysfunction in Type 2 Diabetes.The JNK pathway as a therapeutic target for diabetes.Investigational agents that protect pancreatic islet beta-cells from failure.Chronic pulsatile hyperglycemia reduces insulin secretion and increases accumulation of reactive oxygen species in fetal sheep islets.Thioredoxin-interacting protein: a critical link between glucose toxicity and beta-cell apoptosis.Metabolic syndrome: psychosocial, neuroendocrine, and classical risk factors in type 2 diabetes.Diabetes associated cell stress and dysfunction: role of mitochondrial and non-mitochondrial ROS production and activity.Update on the protective molecular pathways improving pancreatic beta-cell dysfunction Glucolipotoxicity: fuel excess and beta-cell dysfunction.The role of peroxisome proliferator-activated receptor γ in pancreatic β cell function and survival: therapeutic implications for the treatment of type 2 diabetes mellitus.

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A role for glutathione peroxidase in protecting pancreatic beta cells against oxidative stress in a model of glucose toxicity.

http://www.wikidata.org/entity/Q34156113

description

2002 nî lūn-bûn

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2002 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

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2002 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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A role for glutathione peroxid ...... n a model of glucose toxicity.

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A role for glutathione peroxid ...... n a model of glucose toxicity.

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A role for glutathione peroxid ...... n a model of glucose toxicity.

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A role for glutathione peroxid ...... n a model of glucose toxicity.

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A role for glutathione peroxid ...... n a model of glucose toxicity.

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A role for glutathione peroxid ...... n a model of glucose toxicity.

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A role for glutathione peroxid ...... n a model of glucose toxicity.

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A role for glutathione peroxid ...... n a model of glucose toxicity.

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A role for glutathione peroxid ...... n a model of glucose toxicity.

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Proceedings of the National Academy of Sciences of the United States of America

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A role for glutathione peroxid ...... n a model of glucose toxicity.

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Jamie Harmon

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Phuong Oanh T Tran

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R Paul Robertson

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Yoshito Tanaka

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P2860

A simplified system for generating recombinant adenoviruses

Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation

Single-Step Method of RNA Isolation by Acid Guanidinium Thiocyanate–Phenol–Chloroform Extraction

Involvement of protein kinase C beta 2 in c-myc induction by high glucose in pancreatic beta-cells

Prostaglandin E(2) mediates inhibition of insulin secretion by interleukin-1beta

Induction of c-Myc expression suppresses insulin gene transcription by inhibiting NeuroD/BETA2-mediated transcriptional activation

Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage

Reduction of insulin gene transcription in HIT-T15 beta cells chronically exposed to a supraphysiologic glucose concentration is associated with loss of STF-1 transcription factor expression

Molecular mechanisms and clinical pathophysiology of maturity-onset diabetes of the young.

High glucose-altered gene expression in mesangial cells. Actin-regulatory protein gene expression is triggered by oxidative stress and cytoskeletal disassembly.

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