Author(s): Robertson RP
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Abstract Mainstays of therapy for type 2 diabetes involve drugs that are insulin-centric, i.e., they are designed to increase insulin secretion and decrease insulin resistance. The usual clinical course for people so treated is to have initially improved glycemic control but over time a need for intensification of drug-based treatment of hyperglycemia. The mechanism for this unrelenting deterioration of beta-cell function is related to chronic oxidative stress. This suggests that drug discovery should not exclusively focus on insulin-centric targets, but also include glucose-centric strategies, such as antioxidant protection of the beta-cell. This may facilitate repair of beta-cells undergoing damage by oxidative stress secondary to chronic hyperglycemia.
This article was published in Discov Med
and referenced in Journal of Molecular and Genetic Medicine