ArticleFEBS open bio2016
Suppression of liver Apo E secretion leads to HDL/cholesterol immaturity in rats administered ethinylestradiol.
Article in FEBS open bio, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors at 2 institutions in 2 countries.
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Abstract
Ethinylestradiol (EE), a main component of the combined oral contraceptive pill, is associated with an increased risk of arterial diseases. However, the toxicity mechanism of EE is poorly understood. In this study, we found that the exposure to EE reduced the serum apolipoprotein E (Apo E) level and high-density lipoprotein (HDL)/cholesterol concentration in adult female rats. Diethylstilbestrol showed the same effects and both reductions were suppressed by coadministration of tamoxifen (TAM). Liver perfusion experiments revealed that the secretion rate of Apo E from the liver was significantly reduced. It is concluded that EE damages the maturation of HDL/cholesterol by delaying Apo E secretion from the liver, and this may lead to an increased risk of arterial diseases, such as atheromas.
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