Cardiovascular disease (CVD) accounts for almost 75% of mortality in subjects with type 2 diabetes (T2DM). The relationship between hypertension, dyslipidaemia and CVD is now well established. However, the precise link between glycaemia and macrovascular complications has remained unclear. There is now emerging evidence that postprandial glucose (PPG) contributes significantly to CVD risk, although to date there are no large scale interventional studies underway which test the hypothesis that targeting PPG will reduce CVD risk. Until recently, there was no consensus about the definition of postprandial hyperglycaemia. The International Diabetes Federation (IDF) has now developed new clinical guidelines for postprandial glucose and recommend that 2-hour post meal glucose levels are kept < 7.8 mmol/L. In the last few years more has become known about the cellular mechanisms triggered in response to glucose excursions which may explain this increased susceptibility to CVD. Recently, investigation into the contribution of PPG to HbA1c in subjects with T2DM, has shown that this is maximal in relatively well controlled diabetic subjects. Hence PPG is emerging as a legitimate therapeutic target to minimise CVD risk. This review addresses the evidence linking postprandial hyperglycaemia to cardiovascular disease, the cellular mechanisms explaining this enhanced risk and a therapeutic strategy to address postprandial glucose excursions.
Keywords: Cardiovascular disease, postprandial glucose, postprandial hyperglycaemia, diabetes, cellular mechanism, all cause mortality
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