Phuong Oanh T. Tran

TL;DR: Evidence is reviewed that patients with type 2 diabetes continually undergo oxidative stress, that elevated glucose concentrations increase levels of reactive oxygen species inβ-cells, that islets have intrinsically low antioxidant enzyme defenses, and that antioxidant drugs and overexpression of antioxidant enzymes protect β-cells from glucose toxicity.

TL;DR: It is concluded that chronic oxidative stress may play a role in glucose toxicity, which in turn may worsen the severity of type 2 diabetes.

TL;DR: The hypothesis that oxidative stress is one mechanism for glucose toxicity in pancreatic islets is supported by observations that glucose and ribose increase islet peroxide accumulation and that the adverse consequences of ribose-induced oxidative stress on insulin mRNA, content, and secretion can be augmented by a glutathione synthesis inhibitor and prevented by increasing islet GPx activity.

TL;DR: It is concluded that hyperlipidemia induced by high-fat feeding affects insulin secretion in islets from hyperglycemic GK rats only, by a mechanism which may involve, at least in part, modulation of UCP-2 expression.

TL;DR: Exogenous PGE2 mediates the inhibitory effects of exogenous IL-1β on β cell function, and EP3, the PGE 2 receptor subtype whose post-receptor effect is to decrease adenylyl cyclase activity and, thereby, insulin secretion, is the dominant mRNA subtype expressed.