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

Philip Newsholme, Kevin N. Keane, Rodrigo Carlessi, Vinicius Cruzat

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)C420-C433
JournalAmerican journal of physiology. Cell physiology
Volume317
Issue number3
DOIs
Publication statusPublished - 1 Sep 2019

Keywords

  • manganese superoxide dismutase
  • oxygen species
  • superoxide dismutase-2
  • uncoupling protein

Fingerprint Dive into the research topics of 'Oxidative stress pathways in pancreatic β-cells and insulin-sensitive cells and tissues: importance to cell metabolism, function, and dysfunction'. Together they form a unique fingerprint.

Cite this