Postprandial dyslipidaemia and diabetes: mechanistic and therapeutic aspects

Purpose of review There has been a resurgence of interest in the role of triglyceride-rich lipoproteins in the development of atherosclerosis and cardiovascular disease, and this is particularly relevant to diabetes mellitus and the postprandial state. Recent findings Recent evidence suggests that insulin resistance in diabetes induces postprandial dyslipidemia by increasing the enterocytic production of chylomicrons and their remnant particles, but an impaired clearance capacity is also involved. Postprandial dyslipidaemia in diabetes induces oxidative stress, inflammation and endothelial dysfunction and this may be compounded by dysglycaemia. New guidelines for managing hypertriglyceridaemia in diabetes have been published, first-line therapies being improved glycaemic control, treatment of other secondary causes of dyslipidaemia and statin therapy, followed by judicious use of fibrates, n-3 fatty acids or niacin. A new role for incretin-based therapies in regulating dyslipidaemia has been identified. Summary Postprandial dyslipidaemia is a pivotal mechanism whereby diabetes can induce and accelerate atherosclerosis. Regulating the plasma concentrations of triglyceride-rich lipoproteins may decrease the cardiovascular complications of diabetes. The mechanisms of action of incretin-based treatments on dyslipidaemia and endothelial dysfunction need further investigation. The efficacy of new therapies targeted at postprandial dysmetabolism in diabetes need to be confirmed, against best current levels of care, in clinical endpoint trials.