linoleic-acid and ethyl-linoleate

The authors report testing the meconium of a newborn for the presence of FAEE. Meconium from a newborn of a woman who acknowledged drinking beer throughout pregnancy was tested. The authors also tested the meconiums of 3 newborns whose mothers did not drink at all while pregnant. The FAEE were extracted from the meconium samples using solid phase extraction (SPE), and were identified and quantitated by gas chromatography with flame ionization detection (FID). For assignment of retention times and determination of individual concentrations, authentic mixtures of FAEE were injected. The total FAEE concentration in the meconium of the alcohol-exposed infant was 13126 ng/g compared to a mean of 410 ng/g in the control meconiums. Also, in this case, palmitic, linoleic, and stearic ethyl esters were found in the alcohol-exposed infant's meconium while they were not found in the unexposed infant's meconium. In a parallel experiment, the authors spiked increasing amounts of ethyl alcohol (0-40mM) into the meconium from a newborn that was not exposed to ethanol in utero. The spiked samples were incubated for 4 hours at 37 degrees C and subsequently assayed for the presence of ethyl linoleate. In these experiments, they document for the first time that FAEE is produced in meconium. If confirmed by large studies, FAEE may become the first neonatal biologic marker for babies at risk for alcohol-related birth defects.

Topics: Alcohol Drinking; Biomarkers; Chromatography, Gas; Ethanol; Fatty Acids; Female; Humans; Infant, Newborn; Infant, Premature; Linoleic Acid; Linoleic Acids; Male; Maternal-Fetal Exchange; Meconium; Palmitic Acid; Pregnancy; Pregnancy Complications; Stearic Acids

In order to determine how dietary linoleate is metabolized, rats were maintained on a chemically defined diet containing 1.6% ethyl linoleate. After 5 weeks the linoleate was replaced by an equal amount of ethyl 9,10,12,13-d4-linoleate. The animals were killed 3 days later and the molar percentage of d4-linoleate and d4-arachidonate were quantified in liver, heart and kidney phospholipids. In liver, 54 and 22.8 mol% respectively of the esterified linoleate and arachidonate was deuteriated. The lower specific activity of arachidonate versus linoleate suggests that desaturation of linoleate, by a 6-desaturase, is not only rate limiting for synthesis of arachidonate but that the amount of newly synthesized arachidonate is insufficient by itself to maintain steady state levels of esterified arachidonate. The molar fraction of deuteriated linoleate in heart and kidney phospholipids was respectively 35 and 37.4%. These values are lower than for liver phospholipids but it appears there is adequate dietary linoleate available in these tissues for the synthesis of arachidonate. However, of the esterified arachidonate in heart and kidney phospholipids only 4.2 and 8.6 mol% respectively was deuteriated. Our results suggest that arachidonate is made in liver and transported to heart and kidney.

Topics: Animals; Arachidonic Acid; Dietary Fats; Kidney; Linoleic Acid; Linoleic Acids; Liver; Male; Myocardium; Phospholipids; Rats; Rats, Sprague-Dawley

Topics: Animals; Arteriosclerosis; Atherosclerosis; Cholesterol; Diet; Diet, Atherogenic; Linoleic Acid; Linoleic Acids; Lipid Metabolism; Pathology; Pharmacology; Rabbits; Research

Topics: Linoleic Acid; Linoleic Acids; Lipidoses; Liver Cirrhosis; Liver Cirrhosis, Biliary