Abstract

Summary Coronary heart disease (CHD) is the leading cause of death worldwide, and dietary fat intake is one of the major environmental risk factors implicated in its causation. In the drive to prevent CHD, much attention has focused on reducing the amount of energy derived from fat in the diet. However, little attention has been given to the amount of fat consumed in an individual meal and its postprandial effects. Postprandial lipaemia is the term used to describe the series of metabolic events that occur following the consumption of a fatty meal. The extent of postprandial lipaemia is indicated by the size or duration of the increase in plasma triacylglycerol (TAG) concentrations. There is evidence to indicate that exaggerated postprandial lipaemia is linked to an increased risk of CHD. There are several mechanisms by which it may influence the pathological processes that result in CHD, including effects on lipoproteins involved in atherosclerosis and acute effects on haemostatic function. The postprandial response to dietary fat is influenced by non‐dietary factors (such as age, gender and activity level) as well as background diet and the amount and type of fat consumed in a meal. This review focuses on the mechanisms linking postprandial lipaemia and CHD risk and the factors affecting the level of postprandial lipaemia.

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