Abstract
Metabolic and hormonal influences on liver lipid synthesis are reflected in the relative fatty acid composition of serum lecithin. Thus, a sucessive decrease in essential fatty acids (EFA), i.e. n-6 fatty acids, during pregnancy would indicate an incipient EFA deficiency at the time of delivery. Furthermore, reciprocal changes in linoleic and arachidonic acids during the 1st trimester with an increase in arachidonic acid would suggest an enhancement of the Greenbeg Pathway (Pathway II) in lecithin synthesis presumably caused by estrogen influence. During the 2nd and 3rd trimester, reciprocal changes in lecithin content of palmitic and stearic acids are similar to changes appearing under cholestasis.
It is furthermore suggested that variations in the utilization of linoleic acid in cholesterol esters (expressed as cholesterol ester 18:2/lecithin 18:2) might reflect changes in plasma cholesterol esterification by the enzyme lecithin-cholesterol-acyl-transferase (LCAT). Then, in late pregnancy, in relation to a subclinical cholestatic liver engagement, LCAT activity would increase as judged from this ratio as well as the increased linoleic acid in cholesterol esters.