Oxidative stress pathways in pancreatic β-cells and insulin-sensitive cells and tissues: importance to cell metabolism, function, and dysfunction

It is now accepted that nutrient abundance in the blood, especially glucose, leads to the generation of reactive oxygen species (ROS), ultimately leading to increased oxidative stress in a variety of tissues. In the absence of an appropriate compensatory response from antioxidant mechanisms, the cel...

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Veröffentlicht in:American Journal of Physiology: Cell Physiology Jg. 317; H. 3; S. C420
Hauptverfasser: Newsholme, Philip, Keane, Kevin N, Carlessi, Rodrigo, Cruzat, Vinicius
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.09.2019
Schlagworte:
Animals
Diabetes Mellitus, Type 2 - metabolism
Energy Metabolism - physiology
Humans
Insulin - metabolism
Insulin Resistance - physiology
Insulin-Secreting Cells - metabolism
Oxidative Stress - physiology
Reactive Oxygen Species - metabolism
Signal Transduction - physiology
manganese superoxide dismutase
superoxide dismutase-2
oxygen species
uncoupling protein
ISSN:1522-1563, 1522-1563
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Zusammenfassung:It is now accepted that nutrient abundance in the blood, especially glucose, leads to the generation of reactive oxygen species (ROS), ultimately leading to increased oxidative stress in a variety of tissues. In the absence of an appropriate compensatory response from antioxidant mechanisms, the cell, or indeed the tissue, becomes overwhelmed by oxidative stress, leading to the activation of intracellular stress-associated pathways. Activation of the same or similar pathways also appears to play a role in mediating insulin resistance, impaired insulin secretion, and late diabetic complications. The ability of antioxidants to protect against the oxidative stress induced by hyperglycemia and elevated free fatty acid (FFA) levels in vitro suggests a causative role of oxidative stress in mediating the latter clinical conditions. In this review, we describe common biochemical processes associated with oxidative stress driven by hyperglycemia and/or elevated FFA and the resulting clinical outcomes: β-cell dysfunction and peripheral tissue insulin resistance.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
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ISSN:1522-1563
1522-1563
DOI:10.1152/ajpcell.00141.2019