British Journal of Nutrition. 2007;98(3):458-473
Most of diurnal time is spent in a postprandial state due to successive meal intakes along the day. As long as meals contain enough fat, transient increase in triglyceridemia and change in lipoprotein pattern occurs. The extent and kinetics of such postprandial changes are highly variable and are modulated by numerous factors.
This review focuses on factor affecting postprandial lipoprotein metabolism and genes, their variability and their relationship with intermediate phenotypes and coronary heart disease (CHD). Postprandial lipoprotein metabolism is modulated by background dietary pattern as well as meal composition and also by several lifestyle conditions (physical activity, smoking and alcohol consumption), physiological factors (age, gender, menopausal status) and pathological conditions (diabetes mellitus, insulin resistance, obesity). Several lines of evidence suggest that postprandial lipaemia increases the risk of atherogenesis and the roles of many genes have been explored in order to establish the possible implications of their variability in CHD risk.
The postprandial lipid response has been shown to be modified by polymorphisms within the genes for apo AI, apo E, apo B, apo CI, apoCIII, apo AIV, apo AV lipoprotein lipase, hepatic lipase, FABP-2, the fatty acid transport proteins, microsomal triglyceride transfer protein and scavenger receptor class B type I. Future studies will need to be large if they are to assess the effects of multiple polymorphisms. In conclusion, the variability in postprandial lipid response is important and complex but meal composition is one of the key determinants.
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