It has been proposed that pancreatic beta-cell dysfunction in type 2 diabetes is promoted by
oxidative stress caused by NADPH oxidase (Nox) over-activity. The aim of the present study …

Aims/hypothesis Upregulation of the reactive oxygen species (ROS)-producing enzyme
NADPH oxidase (NOX)-1 in islets and beta cells follows acute exposure to inflammatory …

In type 2 diabetes, it has been proposed that pancreatic beta-cell dysfunction is promoted by
oxidative stress caused by NADPH oxidase (NOX) overactivity. Five different NOX enzymes …

Increased intracellular generation of reactive oxygen species [ROS] has been implicated in
the pathology of metabolic [diabetes] and neurodegenerative [Alzheimer's] diseases …

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 …

High glucose-induced oxidative stress and increased NADPH oxidase-2 (NOX2) activity
may contribute to the progressive decline of the functional β-cell mass in type 2 diabetes. To …

Phagocyte-like NADPH oxidase (Nox2) has been shown to play regulatory roles in the
metabolic dysfunction of the islet β-cell under the duress of glucolipotoxic conditions and …

Defects in insulin secretion by pancreatic cells and/or decreased sensitivity of target tissues
to insulin action are the key features of type 2 diabetes. It has been shown that excessive …

In type 2 diabetes, pancreatic β-cells cannot secret enough insulin compensate for insulin
resistance, which are often accompanied by abnormality in lipid metabolism such as …

Background/Aims: Type 1 diabetes (T1D) is characterized by absolute insulin deficiency due
to destruction of pancreatic β-cells by cytokines (eg, interleukin-1β; IL-1β) released by …