RP Robertson, J Harmon, PO Tran, Y Tanaka, H … - Diabetes, 2003 - Am Diabetes Assoc Chronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible
over time, a process that is termed glucose toxicity. Our perspective about glucose toxicity as
it pertains to the pancreatic β-cell is that the characteristic decreases in insulin synthesis ... Cited by 315 - Related articles - BL Direct - All 10 versions
Y Tanaka, POT Tran, J Harmon, RP … - Proceedings of the …, 2002 - National Acad Sciences Antioxidant drugs have been reported to protect pancreatic islets from the adverse effects of chronic
exposure to supraphysiological glucose concentrations. However, glucose has not been shown
to increase intracellular oxidant load in islets, nor have the effects of increasing or ... Cited by 115 - Related articles - BL Direct - All 10 versions
- ►pnas.org Y Tanaka, CE Gleason, POT Tran, JS … - Proceedings of the …, 1999 - National Acad Sciences Chronic exposure of pancreatic islets to supraphysiologic concentrations of glucose causes adverse
alterations in β cell function, a phenomenon termed glucose toxicity and one that may play a
secondary pathogenic role in type 2 diabetes. However, no mechanism of action has ... Cited by 206 - Related articles - BL Direct - All 10 versions
RP Robertson, H Zhou, T Zhang, JS Harmon - Cell biochemistry and …, 2007 - Springer Abstract Type 2 diabetes is characterized by a relentless decline in pancreatic islet beta cell
function and worsening hyperglycemia despite optimal medical treatment. Our central hypothesis
is that residual hyperglycemia, espe- cially after meals, generates reactive oxygen ... Cited by 28 - Related articles - BL Direct - All 4 versions
K Sakai, K Matsumoto, T Nishikawa, M Suefuji, K … - … and biophysical research …, 2003 - Elsevier Pancreatic β-cells exposed to hyperglycemia produce reactive oxygen species (ROS). Because
β-cells are sensitive to oxidative stress, excessive ROS may cause dysfunction of β-cells. Here
we demonstrate that mitochondrial ROS suppress glucose-induced insulin secretion ... Cited by 132 - Related articles - BL Direct - All 6 versions
RP Robertson, J Harmon, POT Tran, V Poitout - Diabetes, 2004 - Am Diabetes Assoc The relentless decline in β-cell function frequently observed in type 2 diabetic patients, despite
optimal drug management, has variously been attributed to glucose toxicity and lipotoxicity. The
former theory posits hyperglycemia, an outcome of the disease, as a secondary force that ... Cited by 202 - Related articles - BL Direct - All 5 versions
M Tiedge, S Lortz, J Drinkgern, S Lenzen - Diabetes, 1997 - Am Diabetes Assoc Antioxidant enzyme expression was determined in rat pancreatic islets and RINm5F insulin-producing
cells on the level of mRNA, protein, and enzyme activity in comparison with 11 other rat
tissues. Although superoxide dismutase expression was in the range of 30% of the liver ... Cited by 333 - Related articles - BL Direct - All 6 versions
JL Evans, ID Goldfine, BA Maddux, GM Grodsky - Diabetes, 2003 - Am Diabetes Assoc In both type 1 and type 2 diabetes, diabetic complications in target organs arise from chronic
elevations of glucose. The pathogenic effect of high glucose, possibly in concert with fatty
acids, is mediated to a significant extent via increased production of reactive oxygen ... Cited by 371 - Related articles - BL Direct - All 10 versions
V Poitout, Y Tanaka, G Reach, RP … - … DE DIABETOLOGIE DE …, 2001 - journees.hotel-dieu.com Le diabète de type 2 (non insulinodépendant) est un syndrome bipolaire associant une résistance
à l'insuline, liée en particulier à l'obésité, et une incapacité du pancréas à y faire face [1, 2]. Son
apparition est déterminée par des facteurs génétiques et des facteurs environnementaux. ... Related articles - View as HTML - BL Direct
RP Robertson - Journal of Biological Chemistry, 2004 - ASBMB Glucose in chronic excess causes toxic effects on structure and function of organs, including
the pancreatic islet. Multiple biochemical pathways and mechanisms of action for glucose toxicity
have been suggested. These include glucose autoxidation, protein kinase C activation, ... Cited by 223 - Related articles - BL Direct - All 6 versions
