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PubMed1999

Oxidation of an oil rich in docosahexaenoic acid compared to linoleic acid in lactating women.

BACKGROUND: We studied the oxidation of an oil rich in docosahexaenoic acid (DHA; DHASCO((R))) in lactating mothers receiving a dietary DHA supplement or a placebo. The results were compared with the oxidation of linoleic acid. METHODS: Breast-feeding mothers received a dietary supplement (DHASCO; 200 mg DHA/day, n = 5) or a placebo (n = 5) for 14 days. Six weeks post partum all 10 mothers received a single dose of 2 mg/kg body weight uniformly (13)C-labeled DHASCO. In a previously reported study 6 mothers received 1 mg/kg body weight uniformly (13)C-labeled linoleic acid. Breath samples were collected over 48 h after tracer application. The total CO(2) production was measured by indirect calorimetry and the (13)C isotopic enrichment of labeled CO(2) by isotopic ratio mass spectrometry. RESULTS: The oxidation of (13)C-labeled DHASCO in the supplemented and placebo groups was similar. Maximal (13)C enrichment was reached earlier in the group receiving (13)C-DHASCO (median 1.0 vs. 3.0 h in the linoleic acid group). The cumulative (13)C recovery in breath was higher in the DHASCO versus the linoleic acid group until 10 h after tracer application and comparable thereafter. CONCLUSIONS: The difference in oxidation of DHASCO versus linoleic acid after tracer ingestion might be partly due to a faster absorption and oxidation of shorter chain saturated fatty acids contained in DHASCO. The cumulative oxidation of DHASCO and linoleic acid 24 and 48 h after tracer ingestion is similar.

Adult↗
PubMed2004

Influence of dietary conjugated linoleic Acid and fat source on body fat and apoptosis in mice.

OBJECTIVE: To determine whether altered dietary essential fatty acid (linoleic and arachidonic acid) concentrations alter sensitivity to conjugated linoleic acid (CLA)-induced body fat loss or DNA fragmentation. RESEARCH METHODS AND PROCEDURES: Mice were fed diets containing soy oil (control), coconut oil [essential fatty acid deficient (EFAD)], or fish oil (FO) for 42 days, and then diets were supplemented with a mixture of CLA isomers (0.5% of the diet) for 14 days. Body fat index, fat pad and liver weights, DNA fragmentation in adipose tissue, and fatty acid profiles of adipose tissue were determined. RESULTS: The EFAD diet decreased (p < 0.05) linoleic and arachidonic acid in mouse adipose tissue but did not affect body fat. Dietary CLA caused a reduction (p < 0.05) in body fat. Mice fed the EFAD diet and then supplemented with CLA exhibited a greater reduction (p < 0.001) in body fat (20.21% vs. 6.94% in EFAD and EFAD + CLA-fed mice, respectively) compared with mice fed soy oil. Dietary FO decreased linoleic acid and increased arachidonic acid in mouse adipose tissue. Mice fed FO or CLA were leaner (p < 0.05) than control mice. FO + CLA-fed mice did not differ in body fat compared with FO-fed mice. Adipose tissue apoptosis was increased (p < 0.001) in CLA-supplemented mice and was not affected by fat source. DISCUSSION: Reductions in linoleic acid concentration made mice more sensitive to CLA-induced body fat loss only when arachidonic acid concentrations were also reduced. Dietary essential fatty acids did not affect CLA-induced DNA fragmentation.

Adipose Tissue↗
PubMed1988

The wormicidal substances of fresh water fishes on Clonorchis sinensis VII. The effect of linoleic acid and ethyl linoleate on parasite viability.

In an attempt to analyze the clonorchicidal activity of linoleic acid and ethyl linoleate in vitro, the wormicidal effects on Clonorchis sinensis were chronologically monitored in dose titration experiments. Excysted metacercariae were killed within a period of 31.0+/-4.0 min, 149.3+/-4.l min and 207.0+/-13.5 min with 100.0 mg, 0.1 mg and 0.001 mg linoleic acid, respectively. The time required for the linoleic acid to kill adult worms was 167.0+/-0.8 min with 100.0 mg, 253.0+/-0.8 min with 0.1 mg, and 277.0+/-0.8 min at 0.001 mg titration. Clonorchicidal activity of ethyl linoleate was relatively delayed as death was observed within 263.3+/-2.9 min, 286.0+/-0.5 min, and 318.0+/-0.8 min for 100.0 mg/ml, 0.1 mg/ml and 0.001 mg/ml concentrations, respectively. The wormicidal effects observed with these pure anticlonorchal substances were found to be similar to the biological activity of native products derived from the mucus of the fresh water fish.

Journal Article↗
PubMed1994

Conjugated linoleic acid (9,11- and 10,12-octadecadienoic acid) is produced in conventional but not germ-free rats fed linoleic acid.

Conjugated linoleic acid (CLA) is an anticarcinogen in several model animal systems. Conjugated linoleic acid occurs naturally in food and is present at higher concentrations in products from ruminant animals. Given that certain rumen microorganisms produce CLA from free linoleic acid, we studied the effect of feeding free or esterified linoleic acid on tissue CLA concentrations using conventional and germ-free rats. Conventional rats were fed a 5% (wt/wt) corn oil control diet alone or supplemented with 5% free linoleic acid or 8.63% corn oil (equivalent to 5% linoleic acid in triglyceride). Germ-free rats were fed autoclavable nonpurified diet alone or supplemented with 5% free linoleic acid. Analyses of CLA concentrations were performed on lipids extracted from liver, lung, kidney, skeletal muscle and abdominal adipose tissue, and on liver phospholipid and neutral lipid fractions. Tissue CLA concentrations were higher in conventional rats fed free linoleic acid (the major isomers were cis-9, trans-11 and trans-9, cis-11) than in control animals. Conjugated linoleic acid concentrations in free linoleic acid-fed rats were maximal at 4 wk, and levels were 5-10 times higher than those of controls. Elevated CLA concentrations were also observed in liver phospholipid and neutral lipid fractions. In contrast, CLA concentrations in the tissues of germ-free rats were not affected by diet. Feeding the corn oil-fortified diet to conventional rats did not increase CLA concentration in the tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed2003

Partial inhibition of biohydrogenation of linoleic acid can increase the conjugated linoleic acid production of Butyrivibrio fibrisolvens A38.

Butyrivibrio fibrisolvens A38, one of the most active rumen bacteria in conjugated linoleic acid (CLA) production, was characterized in vitro. Previous findings that some inhibitory levels of substrate for biohydrogenation (BH) by B. fibrisolvens A38 resulted in more CLA accumulation led to a prediction that partial inhibition of BH could increase ruminal CLA production. The inhibitory conditions for bacterial growth were less effective on the isomerization step than on the following reduction step. Linoleic acid (LA) was inhibitory not only to cell growth but also to LA hydrogenation, and this effect was greater at high concentrations. The reduction step, converting CLA to hydrogenated products (trans-C18:1 and C18:0), was significantly inhibited, and more CLA accumulated during aerobic incubation when LA was added along with a glycolytic inhibitor, iodoacetate (IAA), to cells that were pre-adapted to LA (1 g/OD at 600 nm/L, P < 0.05). Monensin was more inhibitory than IAA to cell growth but less effective for CLA accumulation. Rumen fluid in the culture medium appeared to activate BH even in an aerobic condition, resulting in a lower CLA level than the control group (P < 0.05). Because the isomerization and reduction steps are coupled reactions in BH of most hydrogenating bacteria including B. fibrisolvens A38 cells, both positive and negative modulations of the reduction steps could be key determinants for CLA accumulation in the rumen.

Animals↗
PubMed2003

Dietary conjugated linoleic acid differentially alters fatty acid composition and increases conjugated linoleic acid content in porcine adipose tissue.

Conjugated linoleic acids (CLA) have been shown to decrease body fat content in pigs. It is possible that feeding pigs diets rich in CLA may increase carcass lipid CLA to levels that could provide health benefits when included as a part of a healthy diet. Therefore, the aim of the present study was to determine whether dietary CLA supplementation has any effect on the fatty acid composition of subcutaneous and intramuscular adipose tissue in pigs. Thirty-five female cross bred (Large White x Landrace) pigs (initial weight 57.2 kg and initial P2 back fat 11.5 mm) were used in the present study. Pigs were housed individually and randomly allocated to one of six dietary treatments (0.00, 1.25, 2.50, 5.00, 7.50 and 10.00 g CLA55 (55 g CLA isomers/100 g total fatty acids; Natural Lipids Ltd, Hovdebygda, Norway)/kg) and fed their respective diets for 8 weeks. Twelve CLA isomers in the diet and in pig tissue lipids were separated by Ag+-HPLC. CLA was incorporated at fivefold higher levels in subcutaneous fat as compared with intramuscular fat and in a dose-dependant manner. Overall, the transfer efficiency of CLA was maximized at 5.00 g CLA55/kg. However, there was clear selectivity in the uptake or incorporation of cis,trans-9,11 isomer over the trans,cis-10,12 isomer. In general, CLA supplementation produced significant changes in skeletal muscle and adipose tissue fatty acid composition, indicating that dietary CLA had a potent affect on lipid transport and metabolism in vivo. Significant increases in myristic, palmitic and palmitoleic acids and a reduction in arachidonic acid were observed, suggesting an alteration in activity of delta5-, delta6- and delta9-desaturases in pig adipose tissue. In conclusion, feeding pigs diets supplemented with CLA increases carcass lipid CLA, but also results in changes in the fatty acid profile in pig fat that could potentially outweigh the benefits of CLA.

Adipose Tissue↗
PubMed2003

Effects of highly purified structured lipids containing medium-chain fatty acids and linoleic acid on lipid profiles in rats.

The purpose of this study is to examine the effects of highly purified structured lipids on serum and liver lipid profiles in rats. We also investigated in vitro hydrolysis of lipid emulsions by porcine pancreas. Hydrolysis rates of medium chain (M)-linoleic (L)-medium chain (M) types were 2 to 3 times higher than those of L-M-L types. The diet containing structured lipids or corn oil was administered to rats for 4 weeks. There were no significant differences in growth and food efficiency. Serum cholesterol levels were significantly lower (P<0.05) in the 2-octanoyl-1,3-dilinoleoyl-glycerol, 2-linoleoyl-1,3-didecanoyl-glycerol, and 2-decanoyl-1,3-dilinoleoyl-glycerol groups than in the corn-oil group. Serum triglyceride levels were significantly lower (P<0.05) in rats fed L-M-L types than those in the other groups. Serum non-esterified fatty acid (NEFA) and beta-hydroxybutylate levels were significantly higher (P<0.01) in rats fed M-L-M types than those of the other groups. These results indicate that the feeding of highly purified L-M-L types could effectively improve serum and liver lipid profiles and that M-L-M types may be a preferable substrate for the pancreas and contribute to energy supply in rats.

3-Hydroxybutyric Acid↗
PubMed1985

Conversion of linoleic acid hydroperoxide to hydroxy, keto, epoxyhydroxy, and trihydroxy fatty acids by hematin.

We have carried out a study of the reaction of 13-hydroperoxy-9-cis,11-trans-octadecadienoic acid (linoleic acid hydroperoxide) with hematin. The major products are erythro-11-hydroxy-12,13-epoxy-9-octadecenoic acid, threo-11-hydroxy-12,13-epoxy-9-octadecenoic acid, 9,12,13-trihydroxy-10-octadecenoic acid, 13-keto-9,11-octadecadienoic acid, and 13-hydroxy-9,11-octadecadienoic acid. Several minor products have also been identified, including 9-hydroxy-12,13-epoxyoctadecenoic acid, 11-hydroxy-9,10-epoxy-12-octadecenoic acid, 9-hydroxy-10,12-octadecadienoic acid, and 9-keto-10,12-octadecadienoic acid. Oxygen labeling studies indicate that the observed products arise by at least two pathways. In the major pathway, hematin reduces 13-hydroperoxy-9,11-octadecadienoic acid by one electron to an alkoxyl radical that cyclizes to an adjacent double bond to form an epoxy allylic radical. The allylic radical either couples to the hydroxyl radical coordinated to hematin or diffuses from the solvent cage and couples to O2, forming a peroxyl radical. In the minor pathway, the hydroperoxide is oxidized by one electron to a 13-peroxyl radical that undergoes beta-scission to a pentadienyl radical and O2. Exchange of hydroperoxide-derived O2 for dissolved O2 occurs at this stage followed by coupling of O2 to either terminus of the pentadienyl radical. Both pathways of hydroperoxide metabolism generate significant quantities of peroxyl radicals that epoxidize the isolated double bonds of dihydroaromatic molecules. The products of hydroperoxide reaction with hematin and the oxygen labeling patterns are very similar to the products of unsaturated fatty acid hydroperoxide metabolism by platelets, aorta, and lung. Our results not only provide a mechanism for the formation of a series of mammalian metabolites of linoleic and arachidonic acids but also offer an estimate of the yield of peroxyl radicals generated during the process.

Chemical Phenomena↗
PubMed1982

Linoleic acid in hypertrophic scars.

The relative proportions of the five major fatty acids present in the epidermal polar lipids isolated by swabbing the surface of the skin over hypertrophic scars were compared with the relative proportions observed in normal skin. This comparison necessitates taking the 'normal' sample from unburned skin in an anatomically equivalent area on the patient investigated. When pairs of samples obtained at random from 25 patients attending a pressure therapy clinic with scars of widely differing maturity were analysed, 16 of the 27 sample pairs showed lower levels of essential fatty acid (linoleic acid, C18:2) in phospholipids from over the scarred area compared with the 'area-matched' control normal sample. There did not appear to be any scar-age-related variation in essential fatty acid content. The results suggest that the pathogenesis of hypertrophic scar formation does not necessarily involve a simple overall deficiency of linoleate but that there are considerable differences in the lipid content of epidermis over hypertrophic scars and that of normal skin.

Adolescent↗
PubMed2002

Effect of high-oil corn or added corn oil on ruminal biohydrogenation of fatty acids and conjugated linoleic acid formation in beef steers fed finishing diets.

Three Angus steers (410 kg) cannulated in the proximal duodenum were used in a replicated 3 x 3 Latin square to evaluate the effects of dietary lipid level and oil source on ruminal biohydrogenation and conjugated linoleic acid (CLA) outflow. Dietary treatments included: 1) typical corn (TC; 79.2% typical corn), 2) high-oil corn (HOC; 79.2% high-oil corn), and 3) the TC diet with corn oil added to supply an amount of lipid equal to the HOC diet (OIL; 76.9% TC + 2.4% corn oil). Duodenal samples were collected for 4 d following 10-d diet adaptation periods. Data were analyzed with animal, square, period, and treatment in the model and planned, nonorthogonal contrasts were used to test the effects of dietary lipid content (TC vs HOC and OIL) and oil source (HOC vs OIL) on ruminal biohydrogenation. Intake and duodenal flow of total long-chain fatty acids were increased (P < 0.05) by over 63% for diets containing more lipid regardless of oil source. Apparent ruminal dry matter and long chain fatty acid digestibilities were not altered (P > 0.05) by dietary lipid level or oil source. Ruminal biohydrogenation of total and individual 18-carbon unsaturated fatty acids was greater (P < 0.05) for diets with higher lipid content. Biohydrogenation of oleic acid was greater (P < 0.05) for HOC than OIL, but biohydrogenation of linoleic acid was lower (P < 0.05) for HOC than OIL. Duodenal flows of palmitic, stearic, oleic, linoleic, and arachidic acids were more than 30% greater (P < 0.05) for diets containing more lipid. Flow of all trans-octadecenoic acids was greater (P < 0.05) for diets containing more lipid. Corn oil addition increased (P < 0.05) the flow of trans-10 octadecenoic acid and the trans-10, cis-12 isomer of CLA by threefold compared to feeding high-oil corn. Feeding high-oil corn or adding corn oil to typical corn rations increased intake, biohydrogenation, and duodenal flow of unsaturated long-chain fatty acids. Compared with high-oil corn diets, addition of corn oil increased duodenal flow of trans-10, trans-12 and cis-12 isomers of octadecenoic acid and the trans-10, cis-12 isomer of CLA. The amount of cis-9, trans-11 isomer of conjugated linoleic acid flowing to the duodenum was less than 260 mg/d, a value over 20 times lower than flow of trans-11 vaccenic acid indicating the importance of tissue desaturation for enhanced conjugated linoleic acid content of beef.

Animals↗
PubMed1998

Strong increase in hydroxy fatty acids derived from linoleic acid in human low density lipoproteins of atherosclerotic patients.

Linoleic acid is the most abundant fatty acid in human low density lipoproteins (LDL). Oxidation of LDL transforms linoleic acid to hydroperoxyderivatives. These are converted to 9-hydroxy-10,12-octadecadienoic acid (9-HODE) and 13-hydroxy-9,11-octadecadienoic acid (13-HODE). 9-HODE is much more abundant in oxidized LDL than other lipid peroxidation products and therefore an indicator of lipid peroxidation (LPO). In this study the 9-HODE content in the LDL of 19 obviously healthy volunteers and 17 atherosclerotic patients was investigated. The level of 9-HODE obtained from LDL of young atherosclerotic patients (aged 36-47 years) was increased by a factor of 20 when compared with samples from healthy volunteers of the same age group. The content of 9-HODE in the LDL of atherosclerotic patients aged between 69 and 94 years increased 30-100 fold when compared with young healthy individuals, but when compared with 'healthy' individuals of the same age group it was only 2-3 fold increased. Obviously, as individuals grow older LDL becomes more and more oxidized. Consequently, assuming that LDL oxidation is a precondition for atherosclerosis--older individuals will suffer from atherosclerosis, even if no easy detectable visible signs of this disease are recognizable. According to 9-HODE determination, the onset of the disease starts slowly in most individuals at around 50 years of age.

Adult↗
PubMed1983

[Effect of linoleic acid administration on plasma- and liver lipids. Determination of linoleic acid requirements].

In order to estimate the linoleic acid requirement of the rat, four groups of weanling male Wistar-Rats, 18 animals each, were fed isoenergetic semi-synthetic diets containing 14 cal% fat. The linoleic acid content (as linoleic acid methyl ester) amounted to 0; 0.5; 1.3 and 4.0% of total energy intake. The experiment lasted 14 weeks. The parameters analysed were the concentrations of total lipids (TL), free cholesterol (Ch), cholesterol esters (ChE), triglycerides (TG) and phospholipids (PL) in plasma and liver. - Clinical signs of linoleic acid deficiency were only found in the rats fed the linoleic acid free diet. With 0.5 cal% linoleic acid in the diet no deficiency symptoms were observed. - In plasma of the linoleic acid deficient animals the concentrations of TL, Ch, ChE and TG were decreased. Plasma PL contents were insignificantly altered. - While the contents of TL, TG and ChE in the liver of the deficient rats increased significantly, those of PL and Ch were hardly affected. The results show that a linoleic acid supply of 0.5 cal% prevents nearly all alterations of plasma and liver lipid concentrations noticed in linoleic acid deficiency. The effect of this dose was as good as that of 1.3 cal% linoleic acid. Therefore we assume that the minimum requirement of male young rats for linoleic acid is markedly less than 1,3% of total energy intake.

Animals↗
PubMed1977

Importance of the spleen for the immuno-inhibitory aciton of linoleic acid in mice.

Certain immuno-inhibitory effects of a polyunsaturated fatty acid, linoleic acid (C18:2), no longer occur after splenectomy of young adult CBA mice. This observation suggest that the spleen is a major intermediary in the action of C18:2 on the lymphoreticular system. Pathways of this action remain to be elucidated. Possibilities include C18:2-stimulated suppressor cell generation in the spleen, or excess biosynthesis of immuno-inhibitory prostaglandins by splenic macrophages.

Animals↗
PubMed2003

Linoleic acid, but not oleic acid, upregulates the production of interleukin-8 by human intestinal smooth muscle cells isolated from patients with Crohn's disease.

BACKGROUND & AIMS: Crohn's disease is a chronic inflammatory bowel disease (IBD) of unknown etiology. In this study, we investigated the hypothesis that dietary fatty acids, linoleic acid (LA) and oleic acid (OA), could be involved in the inflammatory response through stimulation of the neutrophil chemokine, IL-8. METHODS: Human intestinal smooth muscle (HISM) cells were isolated from normal patients and patients with Crohn's disease and cultured for 24h with LA or OA in the presence or absence of oxidative stress. The concentrations of IL-8 were measured in the media and cellular oxidative stress was quantitated by measurement of thiobarbituric acid reactive substances (TBARSs). RESULTS: Spontaneous production of IL-8 was significantly higher in HISM cells isolated from Crohn's bowel compared to control bowel. LA caused a marked, nine-fold, increase in IL-8 secretion by Crohn's cells, an effect that could be simulated in normal HISM cells by co-incubation of LA with an oxidizing solution (Ox) composed of hypoxanthine+xanthine oxidase+FeSO(4) (OxLA). These effects were inhibited by vitamins C and E. Treatment of Crohn's cells with OxLA did not further increase IL-8 over that of LA alone. The effect of LA alone was not associated with an increase in cellular oxidative stress as quantitated by TBARSs. In contrast to the results with LA, treatment with OA or OxOA did not increase IL-8 in either normal or Crohn's cells. In addition, OA protected Crohn's cells from the increase in TBARSs induced by Ox. In contrast to IL-8, spontaneous production of monocyte chemotactic protein (MCP-1) was significantly lower in Crohn's HISM cells as compared to normal cells and exposure to OxLA did not increase its production. CONCLUSIONS: LA, but not OA, increased the production of IL-8 by HISM cells. These results suggest that replacement of LA by OA in the diet of Crohn's patients and increased intake of a diet rich in antioxidants could be beneficial in decreasing inflammatory activity in Crohn's disease.

Analysis of Variance↗
PubMed2001

Reduction of linoleic acid inhibition in production of conjugated linoleic acid by Propionibacterium freudenreichii ssp. shermanii.

A method for the production of conjugated linoleic acid (CLA) from linoleic acid (LA) using growing cultures of Propionibacterium freudenreichii ssp. shermanii JS was developed. The growth inhibitory effect of LA was eliminated by dispersing it in a sufficient concentration of polyoxyethylene sorbitan monooleate detergent. For the whey permeate medium used, the optimum LA:detergent ratio was 1:15 (w/w). As a result, the cultures tolerated at least 1000 microg x mL(-1) LA, which was converted to CLA with 57%-87% efficiency. The cis-9, trans-11 and trans-9, cis-11 isomers constituted 85%-90% of the CLA produced. The feasibility of the method was demonstrated also in de Man Rogosa-Sharpe (MRS) broth.

Bacteriological Techniques↗
PubMed1983

Acyl group distributions in tissue lipids of rats fed evening primrose oil (gamma -linolenic plus linoleic acid) or soybean oil (alpha-linolenic plus linoleic acid).

Three groups of rats were fed diets with either 10 weight percent (wt%) of evening primrose oil, safflower oil or soybean oil for 11 weeks. Diets contained 7.1 wt% linoleic acid + 0.8 wt% gamma-linolenic acid, 7.6 wt% linoleic acid, or 5.3 wt% linoleic acid + 0.7 wt% alpha-linolenic acid, respectively. In liver mitochondria as well as in heart, dietary gamma-linolenic acid did not affect the fatty acid profiles of phosphatidylcholines (PC), phosphatidylethanolamines (PE) or cardiolipins (CL), whereas dietary alpha-linolenic acid caused an increased formation of (n-3) polyunsaturated fatty acids (PUFA). The liver delta 6- and delta 5-desaturase activities determined in vitro were not affected by the dietary fats. In brain PE, which are rich in C22- and C20-(n-3) PUFA, as well as in testes PC and PE, which are rich in (n-6) PUFA, no effects were found from a partial replacement of dietary linoleic acid with gamma-linolenic acid or alpha-linolenic acid. In kidney PC, PE, phosphatidylinositol (PI) and CL, 20:3(n-6) was moderately elevated to ca. 1% following intake of gamma-linolenic acid, whereas partial replacement of linoleic acid with alpha-linolenic acid was followed by increased deposition of 22:6(n-3) in PC and PE of testes and kidney. Thus, no general effect of evening primrose oil on the content of (n-6) PUFA in rat tissue phospholipids was observed, whereas a significant incorporation of gamma-linolenic acid into liver and adipose tissue triglycerides was found.

Animals↗
PubMed2001

Infant plasma trans, n-6, and n-3 fatty acids and conjugated linoleic acids are related to maternal plasma fatty acids, length of gestation, and birth weight and length.

BACKGROUND: Arachidonic acid (AA) and docosahexaenoic acid (DHA) are important for growth and neural development. trans Fatty acids (TFAs) may inhibit desaturation of linoleic acid (LA) and alpha-linolenic acid (ALA) to AA and DHA, respectively. Conjugated linoleic acids (CLAs) also alter lipid metabolism and body fat. OBJECTIVE: We determined the associations of birth outcome with maternal and infant plasma concentrations of TFAs, CLAs, AA, and DHA. DESIGN: In healthy women, we sampled maternal blood at 35 wk gestation (n = 58) and umbilical cord blood at birth (n = 70). RESULTS: Mean (+/- SEM) TFA concentrations (% by wt) in infant plasma were as follows: triacylglycerol, 2.83 +/- 0.19 (range: 0.63-12.79); phospholipid, 0.67 +/- 0.03 (0.11-1.33); and cholesteryl ester, 2.04 +/- 0.01 (0.86-4.24). LA, AA, DHA, TFA, and CLA concentrations in infant phospholipids correlated with the same fatty acid in maternal plasma phospholipids (n = 44; P < 0.05). Infant plasma cholesteryl ester and triacylglycerol TFAs and cholesteryl ester CLAs (r = -0.33, -0.42, and -0.49, respectively) were significantly inversely related to length of gestation. Triacylglycerol and cholesteryl ester AA were positively related to length of gestation (r = 0.41 and 0.37, respectively) and birth weight (r = 0.27 and 0.23, respectively). Inverse correlations occurred between infant plasma TFA and DHA concentrations in triacylglycerols (r = -0.33) and between TFA and AA concentrations in cholesteryl esters (r = -0.23). CONCLUSION: The results suggest possible important effects of TFAs and of AA on fetal growth and length of gestation.

Arachidonic Acid↗