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Scholar Results 1 - 10 of about 101 related to Robertson: β-Cell glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes. (0.11 sec) 

β-Cell glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes


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

Glucose toxicity in β-cells: type 2 diabetes, good radicals gone bad, and the …


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

Pancreatic islet β-cell and oxidative stress: The importance of glutathione …


RP Robertson, JS Harmon - FEBS letters, 2007 - Elsevier
Pancreatic β-cell function continuously deteriorates in type 2 diabetes despite optimal treatment
regimens, which has been attributed to hyperglycemia itself via formation of excess levels of
reactive oxygen species (ROS). Glutathione peroxidase GPx), by virtue of its ability to ...
Cited by 21 - Related articles - All 12 versions

Mechanisms of β-cell death in type 2 diabetes


MY Donath, JA Ehses, K Maedler, DM Schumann, H … - Diabetes, 2005 - Am Diabetes Assoc
A decrease in the number of functional insulin-producing β-cells contributes to the pathophysiology
of type 2 diabetes. Opinions diverge regarding the relative contribution of a decrease in β-cell
mass versus an intrinsic defect in the secretory machinery. Here we review the evidence ...
Cited by 86 - Related articles - BL Direct - All 6 versions

Minireview: Secondary {beta}-Cell Failure in Type 2 Diabetes--A Convergence of …

- endojournals.org
V Poitout, RP Robertson - Endocrinology, 2002 - Endocrine Soc
Chronic hyperglycemia and hyperlipidemia can exert deleterious effects on ß-cell function, respectively
referred to as glucotoxicity and lipotoxicity. Over time, both contribute to the progressive deterioration
of glucose homeostasis characteristic of type 2 diabetes. The mechanisms of glucotoxicity ...
Cited by 329 - Related articles - BL Direct - All 4 versions

Evidence against the involvement of oxidative stress in fatty acid inhibition of …


PC Moore, MA Ugas, DK Hagman, SD Parazzoli, V … - Diabetes, 2004 - Am Diabetes Assoc
Prolonged exposure to elevated levels of fatty acids adversely affects pancreatic β-cell
function. Here we investigated 1) whether ceramide synthesis, which we reported to mediate
fatty acid inhibition of insulin gene expression, also inhibits insulin secretion and 2) ...
Cited by 43 - Related articles - BL Direct - All 7 versions

Chronic oxidative stress as a central mechanism for glucose toxicity in pancreatic …


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

Prevention of oxidative stress by adenoviral overexpression of glutathione-related …


RP Robertson, Y Tanaka, H Takahashi, … - ANNALS-NEW …, 2005 - interscience.wiley.com
Abstract: Chronic exposure to supraphysiologic glucose concentrations causes functional damage
to cells and tissues, a process known as glucose toxicity. Recent research indicates that one
important mechanism for glucose toxicity is oxidative stress. Glucose has been shown to ...
Cited by 13 - Related articles - BL Direct - All 5 versions

ER stress and SREBP-1 activation are implicated in {beta}-cell glucolipotoxicity

- biologists.org
H Wang, G Kouri, CB Wollheim - Journal of cell science, 2005 - jcs.biologists.org
The reduction in insulin secretory capacity and ß-cell mass observed in type 2 diabetes is thought
to be caused by glucolipotoxicity secondary to hyperglycemia and hyperlipidemia. Our aim in
this study was to elucidate the underlying molecular mechanisms. We found a strong ...
Cited by 104 - Related articles - BL Direct - All 7 versions

Diabetes, glucose toxicity, and oxidative stress: A case of double jeopardy for the …


RP Robertson, JS Harmon - Free Radical Biology and Medicine, 2006 - Elsevier
Diabetes is commonly referred to in terms of type 1 and type 2. Both forms involve pancreatic
islet β-cell abnormalities, characterized by death in type 1 and accelerated apoptosis in type
2. The resultant chronic hyperglycemia leads to chronic oxidative stress for all tissues ...
Cited by 63 - Related articles - All 3 versions


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