Fatty Acid Composition Of Serum Lecithin Research Articles

Lipid metabolic studies in oophorectomized women. Effects induced by the addition of norethisterone acetate to two different oestrogens on serum individual phospholipids and serum lecithin fatty acid composition.

Abstract. Norethisterone acetate (NET) was administered to 11 oophorectomized women (mean age 34.5 ± 5.9 years) primed with the 17-C-alkylated ethinyl oestradiol (EOe) and the non-alkylated oestrogen, oestradiol valerate (Oe2V) in separate periods. Blood samples were drawn after 4 weeks without hormonal replacement therapy, after 6 weeks on each oestrogen and after 6 weeks on each oestrogen-progestogen combination. Routine liver function tests were carried out, assessment of individual phosholipids i.e. cephalin, lecithin, lysolecithin and sphingomyelin was done after thin layer chromatography. The relative fatty acid composition of serum and high density lipoprotein lecithin and serum cholesterol ester was determined by gas liquid chromatography. The redistribution of serum individual phospholipids (increase in lecithin and decrease in lysolecithin) induced by both oestrogens was reversed by the addition of NET. This lecithin-lysolecithin shift seen after NET administration could depend on a stimulation of the hepatic lipase with its phospholipase Al-activity. The 17-C-alkylated EOe, but not the non-alkylated Oe2V, caused an increase in palmitic and a decrease in stearic acid in the 1-position of serum lecithin. When NET (like EOe, 17-C-alkylated) was added to EOe, this palmitic-stearic acid shift was further accentuated, and it also appeared when NET was added to Oe2V. It is suggested that the shift in 1-position fatty acids of serum lecithin induced by EOe and NET is a non-hormonal 'drug-effect' linked to their 17-C-alkylation and liver toxicity. The reduction in arachidonic acid of serum lecithin and serum cholesterol ester seen after NET administration is interpreted as an anti-oestrogenic effect which could be mediated by a decreased transformation of linoleic to arachidonic acid in the liver.

Effects induced by two different estrogens on serum individual phospholipids and serum lecithin fatty acid composition.

Eleven oophorectomized women (mean age 34.5 +/- 5.9) received two treatment cycles, one of the 17-C-alkylated ethinyl estradiol 20 microgram per day, and the second of the non-alkylated estrogen, estradiol valerate 2 mg per day for six weeks in separate periods preceded by six weeks without hormonal replacement therapy. Blood samples were drawn before and after six weeks on each estrogen. The samples were assayed for individual phospholipids i.e. cephalin, lecithin, lysolecithin and sphingomyelin after separation of these lipids by thin layer chromatography. The relative fatty acid composition of serum and high density lipoprotein lecithin and serum cholesterol ester was determined by gas liquid chromatography. Both estrogens reversed the symptoms of estrogen deficiency and had similar effects on serum individual phospholipids i.e. causing an increase in lecithin concomitant with a decrease in lysolecithin. It is suggested that this lecithin-lysolecithin shift could depend on an inhibition of the hepatic lipase and its phospholipase A1-activity. Both estrogens increased serum lecithin arachidonic acid without causing any change in linoleic acid (the major essential fatty acid), which indicates that this increase in arachidonic acid could be an estrogenic effect independent of dietary factors. Ethinyl estradiol caused an increase in palmitic and a decrease in stearic acid in the 1-position of serum lecithin while estradiol valerate did not influence these fatty acids at all. This palmitic-stearic acid shift induced by ethinyl estradiol is interpreted as a non-hormonal "drug-effect" linked to the liver toxicity of 17-C-alkylated steroids in spite of the lack of influence on routine liver function tests.

Studies in cholestasis of pregnancy. VI. Fatty acid composition of glycero-phospholipids before and after delivery.

Eight pregnant women, complaining of generalized pruritus with lipoprotein-X (LP-X) in their serum and diagnosed as cases of cholestasis of pregnancy (CP)--were studied during pregnancy and after delivery. Ten women with uncomplicated normal pregnancy served as controls. LP-X, liver function tests and relative fatty acid composition of serum lecithin (determined by gas-liquid chromatography, GLC) were followed. The fatty acid composition in liver and serum lecithin is determined by the synthesis pathways of lecithin in the liver. The faster and quantitatively dominating cytidine-diphosphate diglyceride pathway, pathway I, causes the appearance of lecithin with palmitic acid (16:0) in 1-position and oleic (18:1) or linoleic (18:2) acid in 2-position, while pathway II, with methylation of phosphatidyl-ethanolamine (cephalin) preferentially cases the appearance of lecithin with stearic acid (18:0) in 1-position and arachidonic acid (20:4) in 2-position. Pathway I is enchanced by oestrogenic and pathway II by cholestatic influence. During pregnancy women with CP were characterized in their serum lecithin fatty acid composition by a high palmitic (16:0) and a high oleic (18:1) acid content, in agreement with earlier studies. After delivery, in women with prior CP a decrease in palmitic (16:0) and linoleic (18:2) acids and an increase in stearic (18:0) acid, was interpreted as decreased influence on the major lecithin synthesis pathway I and an enhancement of pathway II. In addition, after delivery in the lactating mother, serum lecithin fatty acid composition data revealed an essential fatty acid (EFA) "consumption." It was earlier shown, that women with previous CP (when studied 8--21 months after delivery) had as judged from their serum lecithin fatty acid composition, a "basic metabolic defect," expressing presumably as estrogen enhanced pathway II of liver lecithin synthesis. In the present study, soon after delivery (on day 4--8) women with prior CP showed, however, less pathway II influence than women with a prior normal pregnancy. This was interpreted as a presistence of the cholestatic influence on liver lecithin synthesis pathways at this short time after delivery. Serum lecithin fatty acid composition appears to be a sensitive variable for the evaluation of metabolic influences in the liver.

Serum Lipids and Fatty Acid Composition of Serum Lecithin in the Non‐Pregnant State in Patients with Previous Cholestasis of Pregnancy

Serum lipids and fatty acid composition of serum lecithin were studied 8-21 months after delivery in 20 non-pregnant women who during their latest pregnancy had presented signs of CP. These women were compared with normal non-pregnant women (n=18) and with patients with cholestasis of pregnancy (CP) (n=28). In the non-pregnant state women with previous cholestasis of pregnancy (CP) showed in serum lecithin a low relative content of palmitic (16:0) and linoleic (18:2) acids and a high portion of stearic acid (18:0). These findings indicate as a basic defect in CP, a reduction in liver lecithin synthesis via pathway I (Kennedy's pathway) in favour of an increased pathway II (Greenberg's pathway). These data further support the hypothesis of increased estrogen activity as an etiological factor in CP. The basic influence by pregnancy on serum lipids and serum lecithin fatty acid composition was the same in women with CP as in women with a normal pregnancy.

Studies in cholestasis of pregnancy. V. Gallbladder disease, liver function tests, serum lipids and fatty acid composition of serum lecithin in the non-pregnant state.

Women from an earlier series of cholestasis of pregnancy (CP) were called for a retrospective study to consider presence of gallstones in the gallbladder (evaluated by cholecystography), liver function tests, serum lipids and lipoproteins and the relative fatty acid composition of serum lecithin (as determined by GLC). The attendance in the retrospective study was 60%. Estimated on the total series (assuming that none of the non-responders would have a positive X-ray), the incidence of gallbladder disease was 23.7%. Among women with previous cholestasis of pregnancy and with a positive X-ray finding no characteristic changes in liver function tests or serum lipids were revealed. The women with positive X-ray had, however, a lower alpha-lipoprotein cholesterol than women with negative X-ray. A characteristic finding among women with positive X-ray was furthermore the low relative content of palmitic acid (16:0) in serum lecithin. Also women with negative X-ray had a lower relative content of palmitic acid than controls. It is suggested that the low palmitic acid content is expressive of an influence on liver lecithin synthesis pathways and that the serum lecithin fatty acid composition reflects similar changes in bile lecithin. The "basic defect" in CP influencing liver lecithin synthesis might be the primary cause for disturbed cholesterol solubility in bile and of the frequent occurrence of gallstones in CP.