Journal article
Oxidative stress pathways in pancreatic beta-cells and insulin-sensitive cells and tissues: importance to cell metabolism, function, and dysfunction
American Journal of Physiology: Cell Physiology, Vol.317(3), pp.C420-C433
01/09/2019
PMID: 31216193
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Source: InCites
Abstract
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.
Details
- Title
- Oxidative stress pathways in pancreatic beta-cells and insulin-sensitive cells and tissues: importance to cell metabolism, function, and dysfunction
- Creators
- Philip Newsholme - Curtin UniversityKevin N. Keane - Curtin UniversityRodrigo Carlessi - Curtin UniversityVinicius Cruzat - Torrens University Australia
- Publication Details
- American Journal of Physiology: Cell Physiology, Vol.317(3), pp.C420-C433
- Publisher
- Amer Physiological Soc
- Number of pages
- 14
- Grant note
- Faculty of Health, Torrens University Australia Curtin University School of Pharmacy and Biomedical Sciences, Curtin Health Innovation Research Institute
- Identifiers
- 991013072491402368
- Copyright
- © 2019 the American Physiological Society.
- Academic Unit
- Faculty of Health
- Language
- English
- Resource Type
- Journal article