Glucose and fatty acids synergize to promote B-cell apoptosis through activation of glycogen synthase kinase 3β independent of JNK activation.
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Endoplasmic reticulum stress and type 2 diabetesA20 Inhibits β-Cell Apoptosis by Multiple Mechanisms and Predicts Residual β-Cell Function in Type 1 Diabetes.Atorvastatin helps preserve pancreatic β cell function in obese C57BL/6 J mice and the effect is related to increased pancreas proliferation and amelioration of endoplasmic-reticulum stress.Valproate pretreatment protects pancreatic β-cells from palmitate-induced ER stress and apoptosis by inhibiting glycogen synthase kinase-3βJNK3 maintains expression of the insulin receptor substrate 2 (IRS2) in insulin-secreting cells: functional consequences for insulin signaling.Murine animal models for preclinical islet transplantation: No model fits all (research purposes).Progression from high insulin resistance to type 2 diabetes does not entail additional visceral adipose tissue inflammation.Therapeutic Approaches for Preserving or Restoring Pancreatic β-Cell Function and Mass.Chronic glucolipotoxic conditions in pancreatic islets impair insulin secretion due to dysregulated calcium dynamics, glucose responsiveness and mitochondrial activity.PPARδ Activation Rescues Pancreatic β-Cell Line INS-1E from Palmitate-Induced Endoplasmic Reticulum Stress through Enhanced Fatty Acid Oxidation.Islet Brain 1 Protects Insulin Producing Cells against LipotoxicityMyristic acid potentiates palmitic acid-induced lipotoxicity and steatohepatitis associated with lipodystrophy by sustaning de novo ceramide synthesis.Failure of the adaptive unfolded protein response in islets of obese mice is linked with abnormalities in β-cell gene expression and progression to diabetesThe regulatory roles of NADPH oxidase, intra- and extra-cellular HSP70 in pancreatic islet function, dysfunction and diabetes.Postprandial Dysmetabolism and Oxidative Stress in Type 2 Diabetes: Pathogenetic Mechanisms and Therapeutic Strategies.Interorgan Crosstalk Contributing to β-Cell Dysfunction.Peritoneal dialysis fluid activates calcium signaling and apoptosis in mesothelial cells.ATF3 expression in cardiomyocytes preserves homeostasis in the heart and controls peripheral glucose tolerance.A delayed proinflammatory response of human preadipocytes to PCB126 is dependent on the aryl hydrocarbon receptor.Testing the plasticity of insulin secretion and β-cell functionin vivo: responses to chronic hyperglycaemia in the sheep
P2860
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P2860
Glucose and fatty acids synergize to promote B-cell apoptosis through activation of glycogen synthase kinase 3β independent of JNK activation.
description
2011 nî lūn-bûn
@nan
2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Glucose and fatty acids synerg ...... independent of JNK activation.
@ast
Glucose and fatty acids synerg ...... independent of JNK activation.
@en
type
label
Glucose and fatty acids synerg ...... independent of JNK activation.
@ast
Glucose and fatty acids synerg ...... independent of JNK activation.
@en
prefLabel
Glucose and fatty acids synerg ...... independent of JNK activation.
@ast
Glucose and fatty acids synerg ...... independent of JNK activation.
@en
P2093
P2860
P1433
P1476
Glucose and fatty acids synerg ...... independent of JNK activation.
@en
P2093
Christopher J Rhodes
Cris M Welling
Erik Zmuda
Ernesto Bernal-Mizrachi
Katsuya Tanabe
M Alan Permutt
Nada A Abumrad
Sara C Martinez
Syed D Hasan
Tsonwin Hai
P2860
P304
P356
10.1371/JOURNAL.PONE.0018146
P407
P577
2011-04-26T00:00:00Z