scholarly journals Probucol decreases apolipoprotein A-I transport rate and increases high density lipoprotein cholesteryl ester fractional catabolic rate in control and human apolipoprotein A-I transgenic mice.

1991 ◽  
Vol 11 (5) ◽  
pp. 1295-1302 ◽  
Author(s):  
T Hayek ◽  
T Chajek-Shaul ◽  
A Walsh ◽  
N Azrolan ◽  
J L Breslow
2004 ◽  
Vol 45 (4) ◽  
pp. 716-728 ◽  
Author(s):  
Ji-Young Lee ◽  
Lorraine Lanningham-Foster ◽  
Elena Y. Boudyguina ◽  
Thomas L. Smith ◽  
Ellen R. Young ◽  
...  

2009 ◽  
Vol 94 (12) ◽  
pp. 4891-4897 ◽  
Author(s):  
Laurence Duvillard ◽  
Guillaume Dautin ◽  
Emmanuel Florentin ◽  
Aline Jeannin ◽  
Jean-Paul Pais de Barros ◽  
...  

Context: The impact of estrogen plus progestin as an oral contraceptive on high density lipoprotein (HDL) apolipoprotein (apo) AI metabolism in humans is poorly understood. Objectives: This study was designed to measure the in vivo effect of Moneva (30 μg ethinylestradiol, 75 μg gestodene) on HDL apoAI production rate and fractional catabolic rate. Design: Using 13C-leucine, we performed two kinetic studies in the fed state in 10 normolipidemic young women, before and 3 months after beginning Moneva. Results: 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 · kg−1; P = 0.05) and 26.5% (14.3 ± 2.7 vs. 11.3 ± 2.2 mg · kg−1 · 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). Conclusion: 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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