Abstract
We sought to test the hypothesis that dietary long-chain n-3 PUFA (LC n-3 PUFA) in fish oil stimulate the gene expression of lipoprotein lipase (LPL) in human adipose tissue (AT). In a randomized, double blind, placebo-controlled, cross-over study, 51 male subjects expressing an atherogenic lipoprotein phenotype (ALP) had their diets supplemented with fish oil for 6 weeks. As we previously reported for this group, supplementation with LC n-3 PUFA produced a decrease in fasting plasma triglyceride (TG) (-35%, P < 0.05), attenuation of the postprandial TG response (area and incremental area under the curve; AUC and IAUC, P < 0.05), and a decrease in small, dense LDL. The present study extended these observations by showing that these changes were accompanied by a marked increase in the concentration of LPL mRNA in adipose tissue (AT-LPL mRNA, +55%, P = 0.003) and post-heparin LPL activity (PH-LPL, +31%, P = 0.036). There was also evidence of an association between LPL gene expression and polymorphism in the apolipoprotein E gene. We conclude that the favorable influence of dietary n-3 PUFA on the ALP may be mediated, in part, through an increase in the plasma activity and gene expression of lipoprotein lipase in human adipose tissue.
Highlights
We sought to test the hypothesis that dietary longchain n-3 PUFA (LC n-3 PUFA) in fish oil stimulate the gene expression of lipoprotein lipase (LPL) in human adipose tissue (AT)
Fish oil can ameliorate the lipid abnormalities associated with this condition by suppressing the overproduction of TG in the liver and reducing the extent of postprandial lipemia [7]
Subnormal post-heparin LPL (PH-LPL) activity has been implicated as a possible cause of enhanced postprandial lipemia in insulin resistant states [23,24,25]
Summary
We sought to test the hypothesis that dietary longchain n-3 PUFA (LC n-3 PUFA) in fish oil stimulate the gene expression of lipoprotein lipase (LPL) in human adipose tissue (AT). While direct evidence for the role of dietary fatty acids and their derivatives as regulators of gene expression in humans is still lacking, it is likely that many of the potentially beneficial effects of long-chain n-3 PUFA (LC n-3 PUFA) on TG metabolism are mediated through the control of gene transcription and post-transcriptional events. Fish oil may induce a reduction in VLDL by suppressing lipogenesis and by enhancing the oxidation of fatty acids, both of which are controlled at the level of gene transcription in the liver [8] While these events will indirectly increase the capacity to clear plasma TG in the postprandial period, as a result of reduced competition for lipoprotein lipase (LPL), LC n-3 PUFA may. Journal of Lipid Research Volume 43, 2002 979 exert direct effects on the removal of TG-rich lipoproteins through stimulation of LPL in peripheral tissues [9]
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