Cardiovascular disease (CVD) accounts for almost 75% of mortality in subjects with type 2 diabetes. There is emerging evidence (epidemiological and There is emerging evidence (epidemiological and experimental studies) that postprandial glucose (PPG) contributes significantly to CVD risk, although to date there are no large scale interventional studies with the primary objective of reducing cardiovascular complications by targeting PPG. There is still continuing debate about the definition of postprandial hyperglycaemia. Moreover, we now know more of the cellular mechanisms being triggered in response to glucose excursions which may offer an explanation to this increased susceptibility to CVD. The contribution of PPG to glycosylated haemoglobin, is predominant in relatively well controlled subjects with type 2 diabetes. Hence, PPG is emerging as a legitimate therapeutic target to minimise CVD risk.
This review looks at the evidence linking postprandial hyperglycaemia to CVD, the cellular mechanisms explaining this enhanced risk and a therapeutic strategy to address PPG.