RELATIVE FATTY-ACID COMPOSITION OF SERUM LECITHIN IN PERIMENOPAUSAL WOMEN USING COMBINED HORMONE REPLACEMENT THERAPY

Citation
G. Samsioe et al., RELATIVE FATTY-ACID COMPOSITION OF SERUM LECITHIN IN PERIMENOPAUSAL WOMEN USING COMBINED HORMONE REPLACEMENT THERAPY, Menopause, 4(4), 1997, pp. 193-196
Citations number
17
Journal title
ISSN journal
10723714
Volume
4
Issue
4
Year of publication
1997
Pages
193 - 196
Database
ISI
SICI code
1072-3714(1997)4:4<193:RFCOSL>2.0.ZU;2-5
Abstract
Objective: The atherogenicity of low-density lipoproteins (LDLs) is gr eatly enhanced when LDL is modified, particularly by oxidation. Experi mental data as well as studies in rabbits and monkeys suggest an anti- oxidant effect of estrogens that results in reduced formation of oxidi zed LDL. Oxidized LDL in plasma is rapidly cleared from the circulatio n by means of scavenger receptors, and it is difficult to demonstrate direct changes using plasma samples only. The oxidative potential for the formation of oxidized LDL is derived from the polyunsaturated fatt y acids of the phospholipid lecithin. For example, an increase in the relative content of linoleic and arachidonic acids in serum lecithin c ould tentatively be regarded as a decrease in the formation of oxidize d LDL. Design: Forty perimenopausal women were given continuous hormon e replacement therapy (HRT) consisting of 2 mg of estradiol daily. Aft er random allocation, levonorgestrel comedication was given as 0.250-m g tablets for 10 days per cycle or was continuously released (0.02 mg/ d) from an intrauterine device (IUD). The relative fatty acid composit ion of serum lecithin was determined by gas-liquid chromatography usin g a capillary column equipped with a flame ionization detector and a c omputerized identification system based on retention times. Results: P olyunsaturated acids in serum lecithin were augmented by both regimes with negligible differences between the oral and the IUD group. Conclu sions: The present results indicate that estradiol in combination with either oral cyclical or continuous-release levonorgestrel inhibits fo rmation of oxidized LDL.