Exaggerated postprandial lipaemia and lower post-heparin lipoprotein lipase activity in middle-aged men

An exaggerated postprandial lipaemic response is thought to play a central role in the development of an atherogenic lipoprotein phenotype, a recognized lipid risk factor for coronary heart disease. A small number of limited studies have compared postprandial lipaemia in subjects of varying age, but have not investigated mechanisms underlying age-associated changes in postprandial lipaemia. In order to test the hypothesis that impaired lipaemia in older subjects is associated with loss of insulin sensitivity, the present study compared the postprandial lipaemic and hormone responses for 9 h following a standard mixed meal in normolipidaemic healthy young and middle-aged men. Lipoprotein lipase (LPL) and hepatic lipase (HL) activities were determined in post-heparin plasma 9 h postprandially and on another occasion under fasting conditions. Postprandial plasma glucose (P<0.02), retinyl ester (indirect marker for chylomicron particles; P<0.005) and triacylglycerol (TAG)-rich lipoprotein (density<1.006 g/ml fraction of plasma) TAG (P<0.05) and retinyl ester (P<0.005) responses were higher in middle-aged men, whereas plasma insulin responses were lower in this group (P<0.001). Fasting and 9 h postprandial LPL and HL activities were also significantly lower in the middle-aged men compared with the young men (P<0.006). In conclusion, the higher incremental postprandial TAG response in middle-aged men than young men was attributed to the accumulation of dietary-derived TAG-rich lipoproteins (density<1.006 g/ml fraction of plasma) and occurred in the absence of marked differences in fasting TAG levels between the two groups. Fasting and postprandial LPL and HL activities were markedly lower in middle-aged men, but lack of statistical associations between measures of insulin response and post-heparin lipase activities, as well as between insulin and measures of postprandial lipaemia, suggest that this lower activity cannot be attributed to lack of sensitivity of lipases to activation by insulin. Alternatively, post-heparin lipase activities may not be good markers for the insulin-sensitive component of lipase that is activated postprandially.