Effect of maternal essential fatty acid supply on fatty acid composition of brain, liver, muscle and serum in 21-day-old rats.
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Adipose Tissue↗
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Effect of formula supplemented with docosahexaenoic acid and gamma-linolenic acid on fatty acid status and visual acuity in term infants.
BACKGROUND: Docosahexaenoic acid is present in high concentration in retina and does not influence visual development in preterm infants. It is still under discussion whether docosahexaenoic acid is important for visual development in term infants. METHODS: Thirty-seven infants fed formula for a median of 14 days were randomized at median age of 25 days to three formulas: a) DHAGF: 0.3 wt% docosahexaenoic acid and 0.5 wt% gamma-linolenic acid; b) DHAF 0.3 wt% docosahexaenoic acid; or c) STF: standard formula without long-chain polyunsaturated fatty acids and 17 breast-fed infants were observed, using blood samples and anthropometric measurements from 1 to 4 months of age. At 4 months, visual acuity was measured by swept steady-state visual evoked potential. A cross-sectional study on 25 breast-fed infants was carried out as a reference group for the analyses. RESULTS: Infants fed the two docosahexaenoic acid-supplemented formula had relative docosahexaenoic acid concentrations in red blood cell phospholipids almost as high as those in breast-fed infants, whereas infants in the standard formula group had significantly lower levels. The addition of gamma-linolenic acid to the formula had a positive effect on red blood cell arachidonic acid levels, compared with levels obtained using fish oil only. Visual acuity was significantly different among all feeding groups (analysis of variance; p = 0.05, means +/- standard deviation: breast-fed, 0.37+/-0.06 logMAR; DHAF and DHAGF combined, 0.40+/-0.07 logMAR; and standard formula 0.44+/-0.07 logMAR. However, there was no statistical difference among the formula groups. In a multiple regression analysis including all formula-fed infants, weight at delivery (p = 0.002), but not type of formula, was significantly associated with visual acuity at 4 months of age. CONCLUSIONS: The addition of docosahexaenoic acid resulted in concentrations in red blood cells at similar levels as those in breast-fed infants, whereas the increase in visual acuity did not reach significance. The addition of gamma-linolenic acid resulted in higher arachidonic acid concentrations in red blood cells.
Anthropometry↗
Restoration of defective cross talk in ssi2 mutants: role of salicylic acid, jasmonic acid, and fatty acids in SSI2-mediated signaling.
The Arabidopsis mutants ssi2 and fab2 are defective in stearoyl ACP desaturase, which causes altered salicylic acid (SA)- and jasmonic acid (JA)-mediated defense signaling. Both ssi2 and fab2 plants show spontaneous cell death, express PR genes constitutively, accumulate high levels of SA, and exhibit enhanced resistance to bacterial and oomycete pathogens. In contrast to constitutive activation of the SA pathway, ssi2 and fab2 plants are repressed in JA-mediated induction of the PDF1.2 gene, which suggests that the SSI2-mediated signaling pathway modulates cross talk between the SA and JA pathways. In this study, we have characterized two recessive nonallelic mutants in the ssi2 background, designated as rdc (restorer of defective cross talk) 2 and rdc8. Both ssi2 rdc mutants are suppressed in constitutive SA signaling, show basal level expression of PR-1 gene, and induce high levels of PDF1.2 in response to exogenous application of JA. Interestingly, while the rdc8 mutation completely abolishes spontaneous cell death in ssi2 rdc8 plants, the ssi2 rdc2 plants continue to show some albeit reduced cell death. Fatty acid (FA) analysis showed a reduction in 16:3 levels in ssi2 rdc8 plants, which suggests that this mutation may limit the flux of FAs into the prokaryotic pathway of glycerolipid biosynthesis. Both rdc2 and rdc8 continue to accumulate high levels of 18:0, which suggests that 18:0 levels were responsible for neither constitutive SA signaling nor repression of JA-induced expression of the PDF1.2 gene in ssi2 plants. We also analyzed SA and JA responses of the fab2-derived shs1 mutant, which accumulates levels of 18:0 over 50% lower than those in the fab2 plants. Even though fab2 shs1 plants were morphologically bigger than fab2 plants, they expressed PR genes constitutively, showed HR-like cell death, and accumulated elevated levels of SA. However, unlike the ssi2 rdc plants, fab2 shs1 plants were unable to induce high levels of PDF1.2 expression in response to exogenous application of JA. Together, these results show that defective cross talk in ssi2 can be restored by second site mutations and is independent of morphological size of the plants, cell death, and elevated levels of 18:0.
Arabidopsis↗
Impaired maternal glucose homeostasis during pregnancy is associated with low status of long-chain polyunsaturated fatty acids (LCP) and essential fatty acids (EFA) in the fetus.
Low status of long-chain polyunsaturated fatty acids (LCP) and essential fatty acids (EFA) in the fetus is associated with less favorable neonatal neurological condition. A 'relative', rather than 'absolute' EFA deficiency might explain this finding. A relative EFA deficiency may derive from impaired maternal glucose homeostasis. We measured fatty acids in umbilical vessels of infants born to 7 mothers with (gestational) diabetes mellitus and of 258 infants born to healthy mothers. Umbilical veins of infants of diabetic mothers had higher omega7 and omega9 fatty acids and DHA deficiency index and lower 20:4omega6 and EFA index. Their umbilical arteries had higher omega7 and omega9 fatty acids, and lower 20:4omega6, LCP and EFA index. We conclude that children born to mothers with poor glucose homeostasis have lower EFA and LCP status, which is consistent with a 'relative deficiency' deriving from augmented de novo fatty acid synthesis from the abundant glucose.
Diabetes, Gestational↗
Effects of calcisorb on fecal bile acids and fatty acids in human volunteers.
The intake of calcium (Ca) is negatively associated with colorectal cancer (crc) risk. The aim of this study was to investigate in a double-blind, placebo-controlled trial, the effects of the Ca-binder Calcisorb, which is given to kidney stone patients with hypercalciuria type I, on risk factors for crc risk, bile acids (BA), and long-chain fatty acids (LCFA) in fecal water. Results show that the concentration of BA and LCFA in fecal water did not change, although the urinary excretion of Ca and magnesium (Mg) and the concentration of Ca and magnesium in fecal water decreased. The daily excretion of BA and LCFA acids decreased significantly (p < 0.05) during the Calcisorb period. In conclusion, binding dietary Ca and Mg with Calcisorb from a diet with a relatively low amount of fat does not enhance the solubility of BA and LCFA in fecal water.
Adult↗
Acute modulation of rat hepatic lipid metabolism by sulphur-substituted fatty acid analogues.
A single oral dose of two 3-thia (3-thiadicarboxylic and tetradecylthioacetic acids) and of 4-thia (tetradecylthiopropionic acid) fatty acids were administered to normolipidemic rats and their effects on lipid metabolism over a 24 hr period were studied. All three thia fatty acids could be detected in plasma 2 hr after treatment. Tetradecylthioacetic and tetradecylthiopropionic acids were detected in different hepatic lipid fractions but were incorporated mainly into hepatic phospholipids. Two hours after administration hepatic mitochondrial beta-oxidation and the total liver level of long-chain fatty acyl-CoA increased with a concomitant decrease in saturated fatty acids, total hepatic malonyl-CoA and plasma triacylglycerol levels in the 3-thia fatty acid groups. Tetradecylthiopropionic acid administration caused a decrease in mitochondrial beta-oxidation and an increase in plasma triacylglycerol at 24 hr. The activities of key lipogenic enzymes were unaffected in all treatment groups. Plasma cholesterol level was reduced only at 8 hr in 3-thiadicarboxylic acid treated rats although 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase was suppressed already at 2, 4, 8 and 12 hr. The results show that thia fatty acids are rapidly absorbed and are systemically available after oral administration but the 3-thia fatty acids reached systemic circulation more slowly and less completely than the 4-thia fatty acid. Very low levels of the thia fatty acids are detected in plasma 24 hr after a single administration. They are incorporated into all hepatic lipid classes, especially phospholipids. Rapid incorporation of a non beta-oxidizable thia fatty acid into hepatic lipids may cause a diversion of other fatty acids from glycerolipid biosynthesis to mitochondrial beta-oxidation. Stimulation of mitochondrial beta-oxidation and suppression of HMG-CoA reductase are primary events, occurring within hours, after 3-thia fatty acid administration. The hypotriglyceridemic effect of the 3-thia fatty acids observed at 2-4 hr is independent of the activities of key lipogenic and triacylglycerol synthesising enzymes.
Animals↗
The effect of essential fatty acid deficiency on the fatty acid composition of different salivary glands and saliva in rats.
The main purpose was to compare the changes in fatty acid composition of lipids induced by essential fatty acid (EFA) deficiency in the rat submandibular, parotid and sublingual glands. Three groups of rats were fed for 28 weeks (1 week gestation, 3 weeks lactation and 24 weeks thereafter) diets containing 7% hydrogenated coconut oil (HCO) (EFA-deficient in both n-6 and n-3), 7% soybean oil (SBO) (control) and 7% safflower oil (SFO) (deficient in n-3). Rats were killed and salivary glands were dissected out. Lipids were extracted and the fatty acid composition of total lipids and phospholipids was determined by gas chromatography-mass spectrometry. The fatty-acid compositional changes indicative of an EFA deficiency, such as decreases in the levels of 18:2 n-6, along with an accumulation of 20:3 n-9, were generally observed in all the salivary glands of rats fed 7% HCO diet. In the submandibular glands, the proportions of 16:1, 18:1 n-9 and 18:1 n-7 were also higher in the HCO-fed group than in the other two groups. There were some differences in the fatty acid composition of the three glands. Total lipids of parotid gland had higher levels of 12:0 and 18:1 n-9 as compared to the other two glands. The levels of 18:0, 20:3 n-9, 20:3 n-6 and 20:4 n-6 were, however, lower in the parotid gland as compared with the other glands. In total phospholipids of rats fed SBO- and SFO-containing diets, the sublingual gland had lower levels of 18:2 n-6 and higher levels of 20:4 n-6 than the parotid or the submandibular. These differences in fatty acid composition may be related to possible differences in chain elongation/desaturation. The changes in fatty acid composition were also reflected in total lipids of plasma, liver and whole saliva of rats fed the various diets. A number of fatty acids were identified in saliva by gas chromatography-mass spectrometry.
Analysis of Variance↗
Dietary marine fatty acids (fish oil) for asthma.
BACKGROUND: Epidemiological studies suggest that a diet high in marine fatty acids (fish oil) may have beneficial effects on inflammatory conditions such as rheumatoid arthritis and possibly asthma. OBJECTIVES: 1. To determine the effect of marine n-3 fatty acid (fish oil) supplementation in asthma. 2. To determine the effect of a diet high in fish oil in asthma. SEARCH STRATEGY: The Cochrane Airways Review Group register was search using the terms: marine fatty acids OR diet OR nutrition OR fish oil OR eicosapentaenoic acid OR EPA. Bibliographies of retrieved trials were searched and fish oil manufacturers contacted. SELECTION CRITERIA: Randomised controlled trials in patients with asthma more than two years of age were included. The study duration had to be in excess of 4 weeks. Double blind trials were preferred, but single-blind and open trials were also reviewed for possible inclusion. Three reviewers read each paper, blind to its identity. Decisions concerning inclusion were made by simple majority. Quality assessment was performed by all three reviewers independently. DATA COLLECTION AND ANALYSIS: The only comparison possible was between marine n-3 fatty acid supplementation and placebo. There were insufficient trials to examine dietary manipulation alone. MAIN RESULTS: Eight randomised controlled trials conducted between 1986 and 1998 satisfied the inclusion criteria. Six were of parallel design and two were cross-over studies. Seven compared fish oil with placebo whilst one compared high dose vs low dose marine n-3 fatty acid supplementation. None of the included studies reported asthma exacerbations, health status or hospital admissions. There was no consistent effect on any of the analyzable outcomes: FEV1, peak flow rate, asthma symptoms, asthma medication use or bronchial hyper reactivity. The single study performed in children also combined dietary manipulation with fish oil supplementation and showed improved peak flow and reduced asthma medication use. There were no adverse events associated with fish oil supplements. REVIEWER'S CONCLUSIONS: There is little evidence to recommend that people with asthma supplement or modify their dietary intake of marine n-3 fatty acids (fish oil) in order to improve their asthma control. Equally, there is no evidence that they are at risk if they do so.
Adult↗
A polymorphism in the human intestinal fatty acid binding protein alters fatty acid transport across Caco-2 cells.
The human intestinal fatty acid binding protein (IFABP) binds long-chain fatty acids in vitro, but its intracellular function has remained speculative. A polymorphism in the gene that encodes IFABP results in an alanine (Ala54) to threonine (Thr54) substitution at codon 54 that alters the in vitro binding affinity of the protein for long-chain fatty acids. To identify potential functional variability between Ala54 and Thr54 IFABP, we established permanently transfected Caco-2 cell lines that express either Ala54 or Thr54 IFABP. We found that Caco-2 cells expressing Thr54 IFABP transport long-chain fatty acids and secrete triglycerides to a greater degree than Caco-2 cells expressing Ala54 IFABP. These results provide the first demonstration that IFABP participates in the intracellular transport of long-chain fatty acids. In addition, the observed increase in transport of fatty acids across cells expressing Thr54 IFABP suggests a plausible physiologic mechanism for our prior observation that Pima Indians with a Thr54 IFABP genotype have increased post-absorptive lipid oxidation rates and are more insulin-resistant than Pimas with a Ala54 IFABP genotype.
Biological Transport↗
New cyclopentenyl fatty acids in Flacourtiaceae. Straight-chain fatty acids and cyclic fatty acids in lipids during maturation of the seeds.
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Chemical Phenomena↗
Fatty acids, calcium soaps of fatty acids, and cottonseeds fed to high yielding cows.
We examined the effects of dietary fat as cottonseed, fatty acids, or calcium soaps of fatty acids in the rations of high yielding lactating cows receiving low forage. Experiments were with isoenergetic, isonitrogenous diets containing equal amounts of forage. Inclusion of up to 510 g/d of fatty acids in the ration enhanced FCM yield. With cottonseed, increased FCM was mainly due to increased fat yield. Dietary fatty acids tended to increase milk in mid and late lactation and to decrease fat percentage. Calcium soaps of fatty acids enhanced FCM, particularly in early lactation. Feeding cottonseed and fatty acids together did not enhance yield. Effects described may be attributed in part to changes in ruminal fermentation in which cottonseed increased acetate concentrations and fatty acids decreased the ratio of acetate and butyrate to propionate and in part to enhanced efficiency of milk yield when fat was included in the ration.
Acetates↗
Difference in hepatic metabolism of long- and medium-chain fatty acids: the role of fatty acid chain length in the production of the alcoholic fatty liver.
Replacement of dietary triglycerides containing long-chain fatty acids (LCFA) by triglycerides containing medium-chain fatty acids (MCFA) markedly reduced the capacity of alcohol to produce fatty liver in rats. After 24 days of ethanol and MCFA, the increase in hepatic triglycerides was only 3 times that of controls, whereas an 8-fold rise was observed after ethanol and LCFA. The triglyceride fatty acids that accumulated in the liver after feeding of ethanol with MCFA contained only a small percentage of the MCFA; their composition also differed strikingly from that of adipose lipids. To study the mechanism of the reduction in steatosis, we compared oxidation to CO(2) and incorporation into esterified lipids of (14)C-labeled chylomicrons or palmitate-(14)C (representing LCFA), and of octanoate-(14)C (as MCFA) in liver slices and isolated perfused livers, in the presence or absence of ethanol. Ethanol depressed the oxidation of all substrates to CO(2); MCFA, however, was much more oxidized and reciprocally much less esterified than LCFA, with a 100-fold difference in the ratio of esterified lipid-(14)C to (14)CO(2). Furthermore, in hepatic microsomal fractions incubated with alpha-glycerophosphate, octanoate was much less esterified than palmitate. This propensity of MCFA to oxidation rather than esterification represents a likely explanation for the reduction in alcoholic steatosis upon replacement of dietary LCFA by MCFA.
Animals↗
Inhibition of mitochondrial fatty acid oxidation in pentenoic acid-induced fatty liver. A possible model for Reye's syndrome.
Rats treated with six to eight doses (80 mg/kg, i.p.) of 4-pentenoic acid, an inhibitor of mitochondrial fatty acid oxidation in vitro, during a 48-hr starvation period developed microvesicular fatty infiltration of the liver similar to that observed in Reye's Syndrome. Hepatic triglycerides were elevated an average of 5-fold, although considerable variability was found between individual rats. Fed rats did not develop fatty liver upon similar treatment with pentenoic acid. Liver mitochondria isolated from rats with pentenoic acid-induced fatty liver showed a persistent inhibition of fatty acid oxidation. Rates of oxidation of palmitoylcarnitine and decanoylcarnitine were decreased about 70%, while that of octanoylcarnitine was decreased 50%. Carnitine-independent oxidation of octanoate was also inhibited. Oxidation rates for substrates other than fatty acids, including glutamate, succinate, pyruvate, and alpha-ketoglutarate, were unaffected. Measurements of flavoprotein reduction in intact mitochondria indicated that neither palmitoylcarnitine nor palmitoyl CoA plus L-carnitine could elicit reduction of acyl-CoA dehydrogenase and electron transferring flavoprotein in mitochondria from rats with pentenoic acid-induced fatty liver. These results support a site of inhibition of mitochondrial beta-oxidation at the level of acyl-CoA dehydrogenase for pentenoic acid treatment in vivo, and they suggest a role for nutritional or hormonal factors in the metabolic disposition of pentenoic acid in vivo and in the development of fatty liver.
Animals↗
Fatty acid binding protein removes fatty acids but not phospholipids from microsomes liposomes and sonicated vesicles.
Evidence is provided in this paper that indicates that fatty acids but not phospholipids are removed from microsomes or artificial membranes (liposomes, unilamellar vesicles) by mouse liver cytosolic preparations enriched with fatty acid binding protein (FABP). The cytosolic proteins can act as acceptors for fatty acids but not for phospholipids of microsomal origin. Direct evidence came when liposomes made of egg yolk phosphatidylcholine, containing both [14C]labeled phospholipids and [1-14C] palmitic acid were incubated with FABP. Using sonicated vesicles as fatty acid or phospholipid donors, mouse liver fatty acid binding protein was capable of binding palmitic acid but not phospholipids. These studies suggest that liver fatty acid binding protein can interact with different kinds of membranes increasing specifically the desorption of fatty acids.
Animals↗
Effect of dietary fatty acids on the postprandial fatty acid composition of triacylglycerol-rich lipoproteins in healthy male subjects.
OBJECTIVE: The aim of the present study was to investigate the effect of trans-18:1 isomers compared to other fatty acids, especially saturates, on the postprandial fatty acid composition of triacylglycerols (TAG) in chylomicrons and VLDL. DESIGN: A randomised crossover experiment where five interesterified test fats with equal amounts of palmitic acid (P fat), stearic acid (S fat), trans-18:1 isomers (T fat), oleic acid (O fat), or linoleic acid (L fat) were tested. SUBJECTS: A total of 16 healthy, normolipidaemic males (age 23+/-2 y) were recruited. INTERVENTIONS: The participants ingested fat-rich test meals (1 g fat per kg body weight) and the fatty acid profiles of chylomicron and VLDL TAG were followed for 8 h. RESULTS: The postprandial fatty acid composition of chylomicron TAG resembled that of the ingested fats. The fatty acids in chylomicron TAG were randomly distributed among the three positions in accordance with the distributions in test fats. Calculations of postprandial TAG concentrations from fatty acid data revealed increasing amounts up to 4 h but lower response curves (IAUC) for the two saturated fats in accordance with previous published data. The T fat gave results comparable to the O and L fats. The test fatty acids were much less reflected in VLDL TAG and there was no dietary influence on the response curves. CONCLUSIONS: The fatty acid composition in the test fats as well as the positional distributions of these were maintained in the chylomicrons. No specific clearing of chylomicron TAG was observed in relation to time.
Adult↗
Interaction of n-3 long-chain polyunsaturated fatty acids with n-6 fatty acids in suckled rat pups.
The addition of long-chain polyunsaturated fatty acids (LCP: C20, and C22) to infant formula may permit fatty acid accretion rates similar to breast-fed infants, and may have long-term outcome benefits, such as improved visual acuity and cognitive development. Although fish oil may provide a source of n-3 LCP, sources of n-6 LCP have been more difficult to identify. The present study evaluates the effects of n-3 and n-6 LCP derived from single-cell oils on liver, plasma, and brain fatty acid levels in a neonatal animal model. Newborn rat pups were suckled for 14 d by dams receiving diets containing n-3 LCP alone or combinations of n-3 LCP and increasing doses of linoleic acid (18:2n-6) or arachidonic acid (20:4n-6). Dietary groups received 2% n-3 LCP and 1, 2, or 5% of either 18:2n-6 or 20:4n-6. The 20:4n-6 source also contained modest levels of 18:2n-6. At the termination of the study, liver, plasma, and brain were obtained from the rat pups and the phospholipid fatty acid profiles determined. The results indicate complex interactions of n-3 and n-6 fatty acids. Groups receiving dietary 20:4n-6 incorporated higher levels of n-6 LCP into tissues than did the groups receiving 18:2n-6. The brain was relatively resistant to changes in fatty acid composition compared with the liver and plasma. As expected, tissue n-3 LCP levels were reciprocally related to n-6 levels. The present results document that single-cell LCP oils are bioavailable in a neonatal animal model. The use of 20:4n-6 is a more effective means of supporting n-6 status than the use of 18:2n-6. These results may have implications for the addition of LCP to infant formula.
Animals↗
Lymphatic absorption of structured glycerolipids containing medium-chain fatty acids and linoleic acid, and their effect on cholesterol absorption in rats.
The effects of various structured triglycerides containing medium-chain (caprylic or capric acids) and long-chain (linoleic acid) fatty acids on fatty acid and cholesterol absorption were studied in lymph-cannulated rats. A considerable portion of capric and caprylic acid was absorbed through the lymph duct, although to a lesser extent than was linoleic acid. Capric and linoleic acid located at the 2-position of 2-decanoyl-1,3-dilinoleoyl-glycerol (18:2/10:0/18:2) and 2-linoleoyl-1,3-didecanoyl-glycerol (10:0/18:2/10:0), respectively, tended to be absorbed more efficiently than those located at the 1- and 3-position or those from tricaprin (10:0/10:0/10:0) or trilinolein (18:2/18:2/18:2). A similar trend was observed when the medium-chain fatty acid was caprylic acid instead of capric acid. Caprylic acid absorption from 2-octanoyl-1,3-dilinoleoyl-glycerol (18:2/8:0/18:2) was significantly greater (p less than 0.05) than from 2-linoleoyl-1,3-dioctanoyl-glycerol (8:0/18:2/8:0) or tricaprylin (8:0/8:0/8:0). Preferential absorption of caprylic and linoleic acid was not observed when the 1 to 2 and the 2 to 1 mixtures of 8:0/8:0/8:0 and 18:2/18:2/18:2, respectively, were administered. The structured lipids did not affect the lymphatic absorption of cholesterol. The results suggest that structured triglycerides composed of medium-chain fatty acids and linoleic acid may be more useful for the treatment of lipid malabsorption than are mixtures of medium-chain triglyceride (MCT) and long-chain triglyceride (LCT).
Absorption↗
Polyethenoid fatty acid metabolism; deposition of polyunsaturated fatty acids in fat-deficient rats upon single fatty acid supplementation.
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Acids↗