Mechanisms of tissue damage in the postprandial state

Abstract

There is increasing evidence that the postprandial state is an important contributing factor to the development of atherosclerosis. In diabetes, the postprandial phase is characterised by a rapid and large increase in blood glucose levels and the possibility that the postprandial hyperglycaemic peaks may be relevant to the pathophysiology of late diabetic complications has recently received much attention. The oral glucose tolerance test, although highly non-physiological, has commonly been used as the model of the postprandial state. Epidemiological studies have shown that, when impaired, oral glucose tolerance is associated with an increased risk of cardiovascular disease, with the glycaemia two hours after the glucose challenge a direct and independent risk factor. Moreover, the possibility that postprandial hyperglycaemia is also a risk factor for cardiovascular disease in diabetic patients has been reported. Most of the cardiovascular risk factors are modified in the postprandial phase in patients with diabetes and are directly affected by an acute increase in glycaemia. The mechanisms through which acute hyperglycaemia exerts its effects may be identified as labile non-enzymatic glycation and production of free radicals. It is likely that the two mechanisms co-operate in causing the disorders induced by acute hyperglycaemia. Correcting the postprandial hyperglycaemia can form part of the strategy for the prevention and management of cardiovascular disease in diabetes.