scholarly journals DHA intake interacts with ELOVL2 and ELOVL5 genetic variants to influence polyunsaturated fatty acids in human milk

2019 ◽  
Vol 60 (5) ◽  
pp. 1043-1049 ◽  
Author(s):  
Yixia Wu ◽  
Yan Wang ◽  
Huimin Tian ◽  
Tong Lu ◽  
Miao Yu ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Breast Milk ◽  
Genetic Variants ◽  
Chinese Han ◽  
Four Levels ◽  
Endogenous Synthesis ◽  
Fatty Acid Elongases

Endogenous synthesis of PUFAs is mediated by genes controlling fatty acid elongases 2 and 5 (ELOVL2 and ELOVL5) and by exogenous DHA intake. Associations between elongases and PUFA levels probably involve genetic variants of ELOVL and changes in DHA intake, but data about their combined effect on PUFA levels are sparse. We hypothesized that each factor would directly affect PUFAs and that interactions between haplotypes and DHA intake would influence PUFAs. We explored four levels of DHA intake in pregnant Chinese Han women and 10 SNPs in the ELOVL genes to determine associations with PUFAs in breast milk. The SNP rs3798713 and 3-SNP haplotype (rs2281591, rs12332786, and rs3798713) in ELOVL2 were associated with linoleic acid (LA) concentrations. However, carriers of the 3-SNP haplotype with higher DHA intake (second quartile: 14.58–43.15 mg/day) had higher concentrations of LA, arachidonic acid, EPA, and DHA compared with the interaction baseline. In ELOVL5, five SNPs (rs2294867, rs9357760, rs2397142, rs209512, and rs12207094) correlated with PUFA changes. Compared with those who had the 5-SNP haplotype C-A-C-G-A and low DHA intake (<14.58 mg/day), carriers with other haplotypes (A-A-C-A-A or C-A-C-A-A) and high DHA intake (≥118.82 mg/day) had increased EPA levels after adjustments for age and BMI. This study showed that maternal genetic variants in ELOVL2 and ELOVL5 were associated with PUFA levels in breast milk and that the combination of SNP haplotypes and higher DHA intake increased PUFA concentrations.

scholarly journals Influence of fatty acid desaturase (FADS) genotype on maternal and child polyunsaturated fatty acids (PUFA) status and child health outcomes: a systematic review

2020 ◽  
Vol 78 (8) ◽  
pp. 627-646 ◽  
Author(s):  
Marie C Conway ◽  
Emeir M McSorley ◽  
Maria S Mulhern ◽  
J J Strain ◽  
Edwin van Wijngaarden ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Breast Milk ◽  
Child Health ◽  
Health Outcomes ◽  
Fatty Acid Desaturase ◽  
Child Health Outcomes ◽  
And Child Health

Abstract Context Polyunsaturated fatty acids (PUFA) are important during pregnancy for fetal development and child health outcomes. The fatty acid desaturase (FADS) genes also influence PUFA status, with the FADS genes controlling how much product (eg, arachidonic acid, eicosapentaenoic acid, and docosahexaenoic acid) is metabolized from the precursor molecules linoleic acid and α-linolenic acid. Objective The current review discusses the influence of FADS genotype on PUFA status of pregnant women, breast milk, and children, and also how FADS may influence child health outcomes. Data sources The Ovid Medline, Scopus, Embase, Cochrane Library, CINAHL Plus, PubMed and Web of Science databases were searched from their inception to September 2018. Data extraction Eligible studies reported FADS genotype and blood concentrations of PUFA during pregnancy, in childhood, breast milk concentrations of PUFA or child health outcomes. Data analysis In pregnant and lactating women, minor allele carriers have higher concentrations of linoleic acid and α-linolenic acid, and lower concentrations of arachidonic acid, in blood and breast milk, respectively. In children, FADS genotype influences PUFA status in the same manner and may impact child outcomes such as cognition and allergies; however, the direction of effects for the evidence to date is not consistent. Conclusion Further studies are needed to further investigate associations between FADS and outcomes, as well as the diet-gene interaction.

scholarly journals Exposure to a Farm Environment During Pregnancy Increases the Proportion of Arachidonic Acid in the Cord Sera of Offspring

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 238 ◽  
Author(s):  
Malin Barman ◽  
Karin Jonsson ◽  
Agnes E. Wold ◽  
Ann-Sofie Sandberg
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Breast Milk ◽  
Acid Composition ◽  
Post Partum ◽  
Maternal Diet ◽  
Circulation System ◽  
Adrenic Acid

Growing up in a farm environment is protective against allergy development. Various explanations have been put forward to explain this association. Fatty acids are regulators of immune function and the composition of fatty acids in the circulation system may affect immune development. Here, we investigate whether the fatty acid composition of cord serum differs for infants born to Farm (n = 26) or non-Farm mothers (n =29) in the FARMFLORA birth-cohort. For comparison, the levels of fatty acids in the maternal diet, serum and breast milk around 1 month post-partum were recorded. The fatty acids in the cord sera from infants born to Farm mothers had higher proportions of arachidonic acid (20:4 n-6) and adrenic acid (22:4 n-6) than those from infants born to non-Farm mothers. No differences were found for either arachidonic acid or adrenic acid in the diet, samples of the serum, or breast milk from Farm and non-Farm mothers obtained around 1 month post-partum. The arachidonic and adrenic acid levels in the cord blood were unrelated to allergy outcome for the infants. The results suggest that a farm environment may be associated with the fatty acid composition to which the fetus is exposed during pregnancy.

FATTY ACID COMPOSITION OF PHOSPHATIDYL ETHANOL-AMINE AND PHOSPHATIDYL SERINE FROM DOG BILE

1964 ◽  
Vol 42 (3) ◽  
pp. 309-316 ◽  
Author(s):  
U. K. Misra ◽  
D. A. Turner
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Stearic Acid ◽  
Palmitic Acid ◽  
Linolenic Acid ◽  
Phosphatidyl Ethanolamine ◽  
Phosphatidyl Serine ◽  
Fatty Acid Analysis

Phosphatidyl ethanolamine and phosphatidyl serine extracted from dog bile have been separated by means of ammonium silicate column chromatography. Concentration of phosphatidyl serine in dog bile is about seven times higher than phosphatidyl ethanolamine. Fatty acid analysis by gas chromatography showed that phosphatidyl ethanolamine contains about 26% palmitic acid, 18% stearic acid, 11% linoleic acid, 2% linolenic acid, 9% arachidonic acid, 3% C22:5 fatty acid, and 6% C22:6 fatty acid. The concentrations of these fatty acids observed in phosphatidyl serine are different; palmitic acid represents about 43%, stearic acid 9%, linoleic acid 24%, linolenic acid a trace amount, and arachidonic acid 5%; C22:5 and C22:6 fatty acids are absent.

scholarly journals Inflammatory response to dietary linoleic acid depends on FADS1 genotype

2019 ◽  
Vol 109 (1) ◽  
pp. 165-175 ◽  
Author(s):  
Maria A Lankinen ◽  
Alexander Fauland ◽  
Bun-ichi Shimizu ◽  
Jyrki Ågren ◽  
Craig E Wheelock ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Acid Composition ◽  
Plasma Lipids ◽  
Fasting Glucose ◽  
Saturated Fatty Acids ◽  
Limited Information

ABSTRACT Background The health benefits of substituting dietary polyunsaturated fatty acids (PUFAs) for saturated fatty acids are well known. However, limited information exists on how the response to dietary intake of linoleic acid (LA; 18:2n–6) is modified by polymorphisms in the fatty acid desaturase (FADS) gene cluster. Objectives The aim of the current study was to test the hypothesis that the FADS1 rs174550 genotype modifies the effect of dietary LA intake on the fatty acid composition of plasma lipids, fasting glucose, and high-sensitivity C-reactive protein (hsCRP). Methods Associations were investigated between genotype, plasma PUFAs, fasting glucose, and hsCRP concentrations in the cross-sectional, population-based Metabolic Syndrome in Men cohort (n = 1337). In addition, 62 healthy men from the cohort who were homozygotes for the TT or CC genotype of the FADS1 rs174550 were recruited to a 4-wk intervention (FADSDIET) with an LA-enriched diet. The fatty acid composition of plasma PUFAs and concentrations of plasma fasting glucose, serum hsCRP, and plasma lipid mediators (eicosanoids and related analogs) were measured at the beginning and end of the 4-wk intervention period. Results In the FADSDIET trial, the plasma LA proportion increased in both genotype groups in response to an LA-enriched diet. Responses in concentrations of serum hsCRP and plasma fasting glucose and the proportion of arachidonic acid (20:4n–6) in plasma phospholipids and cholesteryl esters differed between genotype groups (interaction of diet × genotype, P < 0.05). In TT homozygous subjects, plasma eicosanoid concentrations correlated with the arachidonic acid proportion in plasma and with hsCRP (r = 0.4–0.7, P < 0.05), whereas in the CC genotype there were no correlations. Conclusions Our findings show that the FADS1 genotype modifies metabolic responses to dietary LA. The emerging concept that personalized dietary counseling should be modified by the FADS1 genotype needs to be tested in larger randomized trials. The study was registered at clinicaltrials.gov as NCT02543216.

scholarly journals Effects of Different Doses of Metformin on Serum Fatty Acid Composition in Type 2 Diabetic Rats

2017 ◽  
Vol 5 (1) ◽  
pp. 22-28
Author(s):  
Nazi Aghaalikhani ◽  
Mohammad Taghi Goodarzi ◽  
Zeinab Latifi ◽  
Azam Rezaei Farimani ◽  
Amir Fattahi
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Unsaturated Fatty Acids ◽  
Serum Insulin ◽  
Diabetic Rats ◽  
Glucose Levels ◽  
Different Doses

Background: Several studies have shown association of fatty acids with type 2 diabetes (T2D), as well as metformin effects on blood glucose concentrations through affecting lipid metabolism. Objectives: Since the exact therapeutic mechanism of metformin is not clear, in this study we investigated effects of different doses of metformin on serum fatty acids in rats with T2D. Materials and Methods: Twenty-five adult albino male Wistar rats were divided into the following groups: Healthy, untreated T2D, and T2D rats receiving metformin for 4 weeks with doses of 100, 150, and 200 mg/kg/d. Serum insulin and triglyceride (TG) were measured using commercial kits. Serum total lipids were extracted by the Bligh-Dyer method and then compositions of fatty acids were evaluated using gas chromatograph. Results: Monounsaturated fatty acid (MUFA) levels in T2D rats were lower than those in healthy rats (P < 0.05). We also observed that diabetic rats treated with 100 or 150 mg/kg/d of metformin had higher levels of arachidonic acid and polyunsaturated fatty acids (PUFA) in comparison with the healthy group (P < 0.05). Moreover, the T2D+Met (150 mg/kg) group showed increased levels of MUFA compared with the T2D group. Such a difference was seen in levels of arachidonic acid between the T2D+Met 100 mg/ kg group and untreated T2D group. In the group treated with high doses of metformin (200 mg/kg/d), levels of palmitic acid, palmitoleic acid, and saturated fatty acid (SFA) were higher and levels of oleic acid, linoleic acid, arachidonic acid, MUFA, PUFA, and also SFA/UFA ratio were lower compared with other metformin treated and untreated groups (P < .05). In untreated T2D group, there were positive correlations between glucose levels and linoleic acid and PUFA levels (r = 0.707, P = .049 and r = 0.726, P = .041 respectively). Arachidonic acid levels were positively correlated with glucose levels in T2D rats treated with 100 mg/kg/d of metformin (r = 0.969, P = .031). Conclusions: Our study showed that different doses of metformin could have different effects on serum levels of saturated and unsaturated fatty acids, as 200 mg/kg/d of metformin could increase and decrease saturated and unsaturated fatty acids respectively, while lower doses increased unsaturated fatty acids, particularly arachidonic acid.

Abstract 572: The Effect of Inflammation and Soluble Epoxide Hydrolase Inhibition on Fatty Acid Epoxide Incorporation Into VLDL

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Rachel E Walker ◽  
Olga V Savinova ◽  
Theresa L Pedersen ◽  
John W Newman ◽  
Gregory C Shearer
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Epoxide Hydrolase ◽  
Soluble Epoxide Hydrolase ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Alpha Linolenic Acid ◽  
Lps Treatment

Objective: We have previously observed fatty acid epoxides, a class of potent anti-inflammatory oxylipins, in circulating VLDL. The source of these epoxides is unknown. Cytochrome P450 (CYP450) produces them via oxygenation of polyunsaturated fatty acids (PUFAs), and soluble epoxide hydrolase (sEH) converts them to diols. Our objectives were 1) to investigate if incorporation of epoxides into VLDL occurs via hepatic VLDL synthesis and 2) to determine if incorporation is modulated by inflammation or by inhibition of hepatic sEH. Approach and Results: A 2х2 factorial design was used for treatment assignment. Livers were isolated from rats treated with pro-inflammatory lipopolysaccharide (LPS, 10 mg/kg ip) or saline. AUDA, an inhibitor of sEH (10 μM), was included or excluded in the perfusate (Control, N=3; LPS, N=4; AUDA, N=4; LPS+AUDA, N=4). Livers were perfused for 180 minutes. VLDL was isolated by ultra-centrifugation, then analyzed by LC-MS/MS for oxylipin content. Analyzed epoxides and diols were derived from alpha-linolenic acid (ALA), linoleic acid (LA), arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Two-way ANOVA’s were used with triglyceride concentration as a covariate. Concentrations (nM) are reported as mean [95% CI]. DHA-derived epoxides increased with AUDA treatment (3.91 [3.01, 5.07]) compared to livers without AUDA (2.06 [1.58, 2.67]) (p=0.004), but other epoxides were unchanged by AUDA. EPA and ALA-derived epoxides decreased with LPS treatment (0.32 [0.22, 0.47]; 2.44 [2.07, 2.87]) compared to animals without LPS (0.73 [0.46, 1.16]; 3.28 [2.71, 3.96]) (p=0.01; 0.02). AA and DHA-derived diols decreased with LPS treatment (1.01 [0.82, 1.25]; 0.21 [0.17, 0.26]) compared to animals without LPS (1.46 [1.15, 1.86]; 0.31 [0.24, 0.39]) (p=0.03; 0.03). Conclusions: Treatment with LPS and AUDA have significant effects on incorporation of epoxides and diols into VLDL, supporting hepatic incorporation controlled by inflammation. Inflammation decreased select EPA- and ALA-derived epoxides. In contrast, sEH inhibition increased only DHA-derived epoxides. Surprisingly, in VLDL only epoxides derived from omega-3 fatty acids were affected by either inflammation or inhibition of sEH.

Essential fatty acid requirements in human nutrition

1993 ◽  
Vol 71 (9) ◽  
pp. 699-706 ◽  
Author(s):  
Sheila M. Innis
Keyword(s):  
Fatty Acids ◽  
Central Nervous System ◽  
Nervous System ◽  
Arachidonic Acid ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Docosahexaenoic Acid ◽  
Human Milk ◽  
Linolenic Acid ◽  
Essential Fatty Acid

Arachidonic acid (20:4ω−6) and docosahexaenoic acid (22:6ω−3) are major acyl components of cell membrane phospholipids, and are particularly enriched in the nonmyelin membranes of the central nervous system. Dietary deficiency of linoleic acid (18:2ω−6) and linolenic acid (18:3ω−3) during development has been shown to result in reduced levels of 20:4ω−6 and 22:6ω−3 in the developing central nervous system, and this has been associated with altered learning behaviour and visual function. Synthesis of 20:4ω−6 and 22:6ω−3 depends on the dietary intake of 18:2ω−6 and 18:3ω−3, respectively, and the activity of the fatty acid desaturase–elongase enzymes. Oxidation of 18:2ω−6 and 18:3ω−3 for energy, or direct acylation of 18:2ω−6 into triglycerides, cholesteryl esters, and phospholipids, could also influence the amount of 20:4ω−6 and 22:6ω−3 formed. The tissue levels of 20:4ω−6 and 22:6ω−3, or other (ω − 6) and (ω − 3) fatty acids, compatible with optimum growth and development or health are not known. The amount of preformed 22:6ω−3 in the diet of adults, infants fed various milks or formulae, or animals is reflected in the circulating lipid levels of 22:6ω−3. Human milk levels of (ω − 6) and (ω − 3) fatty acids vary, depending in part on the mother's diet. A valid, scientific approach to extrapolate dietary essential fatty acid requirements from the composition of human milk or the circulating lipids of infants fed different diets has not been agreed on. Current data suggest that fatty acid requirements for development of term-gestation piglet brain and retina are met with 5.0% dietary kcal (1 cal = 4.1868 J) 18:2ω−6 and > 1.0% kcal 18:3ω−3, As in rodents and non-human primates, a diet source of 20:4ω−6 and 22:6ω−3 does not seem essential for the developing piglet central nervous system. However, studies in very premature infants suggest these infants may benefit from a dietary source of 20:4ω−6 and 22:6ω−3. Whether the low 20:4ω−6 and 22:6ω−3 status is due to oxidation of 18:2ω−6 and 18:3ω−3 for energy, the effects of early intravenous feeding with lipid emulsions, rapid growth, or immaturity of physiological or metabolic pathways in very preterm infants is not yet known.Key words: linoleic acid, linolenic acid, arachidonic acid, docosahexaenoic acid, brain, retina.

scholarly journals Studies on the nutrition of marine flatfish. The effect of different dietary fatty acids on the growth and fatty acid composition of turbot (Scophthalmus maximus)

1976 ◽  
Vol 36 (3) ◽  
pp. 479-486 ◽  
Author(s):  
C. B. Cowey ◽  
J. M. Owen ◽  
J. W. Adron ◽  
C. Middleton
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Linolenic Acid ◽  
Scophthalmus Maximus ◽  
Dietary Fatty Acids ◽  
Cod Liver Oil ◽  
Weight Gains

1. Five groups of juvenile turbot (Scophthalmus maximus) which had been given a diet free of fat for 12 weeks were given diets in which the lipid component (g/kg) was: oleic acid alone 50, oleic acid 40+linoleic acid 10, oleic acid 40+linolenic acid 10, oleic acid 40+arachidonic acid 10 or oleic acid 40+cod-liver oil 10. These five experimental diets were given for 16 weeks.2. Weight gains were highest in the group given the diet containing cod-liver oil and lowest in the groups given diets containing oleic acid alone or oleic acid+linoleic acid. Weight gains in the groups given oleic acid+arachidonic acid or linolenic acid were markedly inferior to those of the group given oleic acid+cod-liver oil. It is concluded that arachidonic acid is inferior to polyunsaturated fatty acids of the ω3 series in maintaining growth rate in turbot.3. Fatty acid analyses of neutral lipids and phospholipids of liver and extrahepatic tissues did not suggest any evidence of desaturation of dietary oleic acid, linoleic acid or linolenic acid by the turbot. These experiments confirm previous isotopic evidence that turbot lack the necessary microsomal desaturases to perform this metabolic transformation.

scholarly journals Fatty acid changes in liver and plasma lipid fractions after safflower oil was fed to rats deficient in essential fatty acids

1967 ◽  
Vol 105 (1) ◽  
pp. 343-350 ◽  
Author(s):  
R. R. Johnson ◽  
P. Bouchard ◽  
J. Tinoco ◽  
R. L. Lyman
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Essential Fatty Acids ◽  
Plasma Lipid ◽  
Eicosatrienoic Acid ◽  
Liver Phospholipid ◽  
Safflower Oil

1. Fatty acid patterns of liver and plasma triglycerides, phospholipids and cholesteryl esters were determined at intervals during 24hr. after essential fatty acid-deficient rats were given one feeding of linoleate (as safflower oil). 2. Liver triglyceride, phospholipid and cholesteryl ester fatty acid compositions did not change up to 7hr. after feeding. Between 7 and 10hr., linoleic acid began to increase in all fractions, but arachidonic acid did not begin to rise in the phospholipid until 14–19hr. after feeding. 3. Oleic acid and eicosatrienoic acid in liver phospholipid began to decline at about the time that linoleic acid increased, i.e. about 9hr. before arachidonic acid began to increase. 4. Changes in linoleic acid, arachidonic acid and eicosatrienoic acid in phosphatidylcholine resembled those of the total phospholipid. Phosphatidylethanolamine had a higher percentage content of arachidonic acid before the linoleate was given than did phosphatidylcholine, and after the linoleate was given the fatty acid composition of this fraction was little changed. 5. The behaviour of the plasma lipid fatty acids was similar to that of the liver lipids, with changes in linoleic acid, eicosatrienoic acid and arachidonic acid appearing at the same times as they occurred in the liver. 6. The results indicated that linoleic acid was preferentially incorporated into the liver phospholipid at the expense of eicosatrienoic acid and oleic acid. The decline in these fatty acids apparently resulted from their competition with linoleic acid for available sites in the phospholipids rather than from any direct replacement by arachidonic acid.

scholarly journals Thromboregulation by Platelet Phospholipid Fatty Acids: Effect of Dietary Linoleate

1977 ◽  
Author(s):  
G. Hornstra
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Unsaturated Fatty Acids ◽  
Thrombus Formation ◽  
Platelet Phospholipid ◽  
Platelet Release ◽  
Dietary Linoleate

It is thought that fatty acids, released from certain platelet phospholipids regulate the platelet release reaction and, thereby, thrombus formation. Arachidonic acid (AA) has been shown to be of major importance in this respect, since it is converted by the cyclo-oxygenase (CO-) system to release-inducing substances. However, the AA-CO interaction is inhibited competitively by other poly-unsaturated fatty acids such as linoleic acid (LA). This implies that the ultimate thrombotic response will depend on the ratio between AA and competing fatty acids, released upon platelet activation and, consequently, on the fatty acid composition of certain platelet phospholipids.In rats, the ratio between AA and LA from platelet phosphotidylcholine is found to be negatively related to the dietary LA content. Since phosphotidylcholine has been shown to be the main source of AA, this finding may explain the well-established anti-thrombotic effect of dietary linoleate.

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