Reactive XXXX species as a signal in @entity413 -stimulated insulin secretion.

@entity4250 @entity14625 @entity274 @entity6 @entity43840 @entity19 @entity26 @entity898 @entity224 @entity413 @entity11838
One of the unique features of beta-cells is their relatively low expression of many antioxidant enzymes. This could render beta-cells susceptible to oxidative damage but may also provide a system that is sensitive to reactive @entity26 species as signals. In isolated @entity19 islets and INS-1(832/13) cells, @entity413 increases intracellular accumulation of @entity274 . In both models, insulin secretion could be stimulated by provision of either exogenous @entity274 or @entity43840 , which raises intracellular @entity274 levels. Provision of exogenous @entity274 scavengers, including cell permeable catalase and @entity898 , inhibited @entity413 -stimulated @entity274 accumulation and insulin secretion (GSIS). In contrast, cell permeable @entity224 dismutase, which metabolizes @entity224 into @entity274 , had no effect on GSIS. Because oxidative stress is an important risk factor for beta-cell dysfunction in @entity6 , the relationship between @entity413 -induced @entity274 generation and GSIS was investigated under various oxidative stress conditions. Acute exposure of isolated @entity19 islets or INS-1(832/13) cells to oxidative stressors, including @entity4250 , @entity11838 , and @entity14625 , led to decreased GSIS. This impaired GSIS was associated with increases in a battery of endogenous antioxidant enzymes. Taken together, these findings suggest that @entity274 derived from @entity413 metabolism is one of the metabolic signals for insulin secretion, whereas oxidative stress may disturb its signaling function.
