POSTPRANDIAL HYPERGLYCEMIA

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The incidence of long term complications in diabetes has been strongly linked to glycemic control 1,2,3. Recently there has been significant interest in the role of postprandial hyperglycemia in the development of cardiovascular disease in diabetes 4,5,6. Epidemiological studies show a relationship between the 2hr glucose concentration after an oral load, and cardiovascular risk 7. In addition interventional studies aimed at reducing postprandial glucose concentrations, seem to support the importance of postprandial hyperglycemia as a target for diabetic therapy 8,9. Hyperglycemia has been shown to induce superoxide production by mitochondrial electron transport chain.This has been proposed as the underlying mechanism by which hyperglycemia leads to increased cardiovascular disease 10 F2 isoprostane 8-iso prostaglandin F2alpha, has been shown to be a reliable marker of oxidative stress 11,12. While there is a growing body of evidence in support of the importance of postprandial hyperglycemia as a target for diabetic treatment, many questions remained unanswered. In particular, it is not known whether it is the degree of hyperglycemia, or the duration for which an individual remains hyperglycemic, which results in the oxidative stress seen after a meal.