Abstract
In type 2 diabetes, metabolic stress has a negative impact on pancreatic β-cell function and survival (T2D). Although the pathogenesis of metabolic stress is complex, an imbalance in redox homeostasis causes abnormal tissue damage and β-cell death due to low endogenous antioxidant expression levels in β-cells. Under diabetogenic conditions, the susceptibility of β-cells to oxidative damage by NADPH oxidase has been related to contributing to β-cell dysfunction. Here, we consider recent insights into how the redox response becomes deregulated under diabetic conditions by NADPH oxidase, as well as the therapeutic benefits of NOX inhibitors, which may provide clues for understanding the pathomechanisms and developing strategies aimed at the treatment or prevention of metabolic stress associated with β-cell failure.
Highlights
Type 2 diabetes (T2D) is a complicated metabolic condition marked by peripheral insulin resistance [1], obesity [1], hyperglycemia [2], and elevated levels of cytokines [3], all of which contribute to a lack of insulin and consequent β-cell failure
In this review of the current literature, we focus on the role of NADPH oxidase (NOX) enzymes in signal transduction in pancreatic β-cells, as well as discuss how these cells might contribute to the development of type 2 diabetes
These observations were further supported by using NOX2 knockout mice, suggesting that NOX2-dependent H2O2 production is a likely cause of early palmitate-dependent impairment in insulin secretion and the induction of β-cell dysfunction [82]
Summary
Type 2 diabetes (T2D) is a complicated metabolic condition marked by peripheral insulin resistance [1], obesity [1], hyperglycemia [2], and elevated levels of cytokines [3], all of which contribute to a lack of insulin and consequent β-cell failure. There is strong evidence that suggests that chronically elevated levels of reactive oxygen species (ROS) lead to increased oxidative stress in β-cells. NADPH oxidase (NOX) proteins are membrane-associated multiunit enzymes that play a physiological role in response to various factors, as well as pathophysiological roles in diabetic pancreatic β-cells. In this review of the current literature, we focus on the role of NOX enzymes in signal transduction in pancreatic β-cells, as well as discuss how these cells might contribute to the development of type 2 diabetes
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