Postprandial hypertriglyceridemia induced by saturated vs. monounsaturated fatty acids is related to reduced hepatic lipoprotein receptors binding in NZW rabbits

Conclusions

As compared to a low-fat control diet, chronic ingestion of a SFA diet increased postprandial lipemia, did not noticeably modify lipoprotein lipase and hepatic lipase activities, and decreased binding activities to LDL-R as well as LSR. On the contrary, a MUFA-rich diet did not alter postprandial lipemia, had no effect on lipase activities, but increased binding activities to LDL-R and to LSR measured on hepatocyte plasmic membrane. In both cases, postprandial triglyceridemia and accumulation of triglycerides from dietary origin were inversely correlated to LDL-R and LSR binding activities.

The reduced LDL-R as well as LSR binding activities could explain the postprandial hypertriglyceridemia observed in rabbits chronically ingesting SFA. MUFA could prevent postprandial accumulation of TRL by accelerating their hepatic uptake mediated by LDL-R and LSR.