Abstract

The impact of estrogen plus progestin as an oral contraceptive on high density lipoprotein (HDL) apolipoprotein (apo) AI metabolism in humans is poorly understood. This study was designed to measure the in vivo effect of Moneva (30 microg ethinylestradiol, 75 microg gestodene) on HDL apoAI production rate and fractional catabolic rate. Using (13)C-leucine, we performed two kinetic studies in the fed state in 10 normolipidemic young women, before and 3 months after beginning Moneva. On Moneva, serum triglycerides increased by 12% (P = 0.03) in the fed state, whereas low-density lipoprotein and HDL cholesterol remained unchanged. HDL apoAI pool size and production rate were increased by 9.2% (67.3 +/- 7.1 vs. 61.6 +/- 6.7 mg x kg(-1); P = 0.05) and 26.5% (14.3 +/- 2.7 vs. 11.3 +/- 2.2 mg x kg(-1) x d(-1); P = 0.02), respectively. HDL apoAI fractional catabolic rate was not significantly modified. Three-month treatment by Moneva induced a shift of HDL size distribution from HDL2 toward HDL3 (HDL3 = 51.5 +/- 8.1 vs. 46.5 +/- 9.2% of total HDL; P = 0.02) and an increase in the proportion of apoAI among HDL components (38.8 +/- 4.3 vs. 34.4 +/- 2.8%; P = 0.01). Oral contraception by estrogen plus progestin induces changes in HDL apoAI metabolism characterized by an increase in production rate and pool size, with a higher proportion of HDL3 particles. Whether or not these changes are beneficial to prevent atherosclerosis has to be explored further.

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