Circulating lipoprotein profiles are modulated differently by lipoprotein lipase in obese humans

Background Several genetic analyses have suggested that lipoprotein lipase (LpL) genotypes causing decreased LpL activity correlate with increased tri glyceride concentrations and risk for coronary artery disease. In contrast, in some other studies LpL activity was positively correlated with plasma l ow-density lipoprotein (LDL) cholesterol concentrations. Objective To assess whether these different associations represent physiolo gic differences in lipoprotein metabolism. Methods We correlated postheparin lipase activities, postprandial lipemia, and fasting lipoprotein concentrations in obese (BMI greater than or equal to 30 kg/m(2), n = 26) and non-obese (BMI less than or equal to 30 kg/m(2), n = 57) individuals. LpL was measured using specific inhibitory antibodies . Results Surprisingly, LpL activity was significantly correlated with trigly ceride area under the curve after a fat load in the non-obese, but not the entire group. Moreover, in non-obese individuals, LpL activity correlated d irectly (r = 0.40) and hepatic lipase activity correlated inversely (r = -0 .32) with high-density lipoprotein (HDL) cholesterol concentrations. These relationships were not found in the obese group, in whom LpL correlated wit h LDL cholesterol concentrations (r = 0.54). Conclusions We conclude that postheparin LpL activity relates to different lipoproteins in obese and non-obese individuals. In obesity, greater LpL ac tivity may enhance conversion of very-low-density lipoprotein cholesterol t o LDL cholesterol, whereas in non-obese individuals the correlation is with HDL cholesterol. Whether this is due to differences in the source of LpL ( muscle or fat), or to other associated alterations in lipoprotein metabolis m is unknown. These results may explain the non-uniformity of correlations between LpL and atherogenic lipoproteins in different populations. J Cardio vasc Risk 7: 41-47 (C) 2000 Lippincott Williams & Wilkins.