Database : MEDLINE
Search on : Arachidonic and Acids [Words]
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[PMID]: 29506525
[Au] Autor:Arain SQ; Talpur FN; Channa NA; Ali MS; Afridi HI
[Ad] Address:National Centre of Excellence in Analytical Chemistry, University of Sindh, Jamshoro, 76080, Pakistan.
[Ti] Title:Serum lipids as an indicator for the alteration of liver function in patients with hepatitis B.
[So] Source:Lipids Health Dis;17(1):36, 2018 Mar 05.
[Is] ISSN:1476-511X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Hepatitis B virus (HBV) exerts an intense impact on host lipid metabolism. Hence the aim of present study is to determine metabolic derangement that occurred in subjects suffering from hepatitis B patients. METHODS: The fasting blood samples were collected from hepatitis B patients (n = 50) attended in Taluka hospital TandoAdam, Sindh with age and gender matched controls (n = 50). Serum lipid profile and fatty acid (FA) composition were analyzed by micro-lab and gas chromatography. RESULTS: The hepatitis B patients have significantly lower level (p < 0.01) of lipid profile including total cholesterol (TC), triacylglyceride (TAG), high density lipoprotein-C (HDL-C) very low density lipoprotein-cholesterol (VLDL-C), low density lipoprotein-cholesterol (LDL-C), and total lipid (TL) in comparison to controls, indicating hypolipidemia in patients. The result of total FA composition of HBV patients in comparison to controls reveal that myristic, palmitic, docosahexaenoic acids were significantly (p < 0.05) higher, while linoleic, eicosatrienoic, arachidonic, eicosapentaenoic acids were lower in HBV patients in comparison to controls. The elongase, ∆5 and ∆6-desaturase enzymes activities were found lower, while ∆9-desaturase activity was higher in hepatitis B patients as compared to controls, which indicates the impaired lipid metabolism. CONCLUSION: The serum saturated fatty acid (SFA) and monounsaturated fatty acid (MUFA) were increased while polyunsaturated fatty acid (PUFA) was reduced in both total and free form in hepatitis B patients due to altered activities of enzyme desaturases with impaired PUFA metabolism and non-enzymatic oxidation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1186/s12944-018-0683-y

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[PMID]: 29522918
[Au] Autor:Gurung AB; Mayengbam B; Bhattacharjee A
[Ad] Address:Computational Biology Laboratory, Department of Biotechnology and Bioinformatics, North-Eastern Hill University, Shillong, Meghalaya, 793022, India.
[Ti] Title:Discovery of novel drug candidates for inhibition of soluble epoxide hydrolase of arachidonic acid cascade pathway implicated in atherosclerosis.
[So] Source:Comput Biol Chem;74:1-11, 2018 Mar 06.
[Is] ISSN:1476-928X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Soluble epoxide hydrolase (sEH), a key enzyme belonging to cytochrome P450 pathway of arachidonic acid cascade is a novel therapeutic drug target against atherosclerosis. The enzyme breaks down epoxyeicosatrienoic acid (EETs) to dihydroxy-eicosatrienoic acids (DHETs) and reduces beneficial cardiovascular properties of EETs. Thus, the present work is aimed at identification of potential leads as sEH inhibitors which will sustain the beneficial properties of EETs in vivo. PubChem and ZINC databases were screened for drug-like compounds based on Lipinski's rule of five and in silico toxicity filters. The binding potential of the drug-like compounds with sEH was explored using molecular docking. The top ranked lead (ZINC23099069) showed higher GOLD score compared with that of the control, 12-(3-adamantan-1-yl-ureido)-dodecanoic acid butyl ester (AUDA-BE) and displayed two hydrogen bonds with Tyr383 and His420 and eleven residues involved in hydrophobic interactions with sEH. The apo_sEH and sEH_ZINC23099069 complex showed stable trajectories during 20 ns time scale of molecular dynamics (MD) simulation. Molecular Mechanics Poisson-Boltzmann Surface Area (MM/PBSA) binding free energy analysis showed that electrostatic energy is the driving energy component for interaction of the lead with sEH. These results demonstrate ZINC23099069 to be a promising drug candidate as sEH inhibitor against atherosclerosis instead of the present urea-based inhibitors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  3 / 30406 MEDLINE  
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[PMID]: 29353041
[Au] Autor:Hayashi Y; Shimamura A; Ishikawa T; Fujiwara Y; Ichi I
[Ad] Address:Graduate School of Humanities and Sciences, Ochanomizu University, Tokyo, Japan.
[Ti] Title:FADS2 inhibition in essential fatty acid deficiency induces hepatic lipid accumulation via impairment of very low-density lipoprotein (VLDL) secretion.
[So] Source:Biochem Biophys Res Commun;496(2):549-555, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Fatty acid desaturase 2 (FADS2) is responsible for the first desaturation reaction in the synthesis of highly unsaturated fatty acids (HUFAs), such as arachidonic acid (20:4n-6) and eicosapentaenoic acid (20:5n-3), and is involved in Mead acid (20:3n-9) production during essential fatty acid deficiency (EFAD). In this study, an obvious hepatic lipid accumulation was observed in EFAD mice treated with a FADS2 inhibitor. FADS2 inhibition in the EFAD state reduced secretion of very low-density lipoprotein (VLDL) and markedly diminished Mead acid in phosphatidylcholine (PC) in the liver and plasma. As the results, the amount of C20 HUFAs in hepatic and plasma PC dramatically reduced in the EFAD mice treated with a FADS2 inhibitor, whereas the decrease of C20 HUFA levels of PC in EFAD mice was not observed because of the increased Mead acid in PC. These results supposed that Mead acid in PC is important as a component of VLDL. It is possible that Mead acid plays the role of a substitute of HUFAs in VLDL secretion during EFAD.
[Mh] MeSH terms primary: Fatty Acid Desaturases/metabolism
Fatty Acids, Unsaturated/metabolism
Lipoproteins, VLDL/metabolism
Liver/metabolism
[Mh] MeSH terms secundary: 8,11,14-Eicosatrienoic Acid/analogs & derivatives
8,11,14-Eicosatrienoic Acid/metabolism
Animals
Fatty Acid Desaturases/antagonists & inhibitors
Fatty Liver/metabolism
Lipid Metabolism
Male
Mice, Inbred C57BL
Oxidation-Reduction
Phosphatidylcholines/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Fatty Acids, Unsaturated); 0 (Lipoproteins, VLDL); 0 (Phosphatidylcholines); 7324-41-6 (8,11,14-Eicosatrienoic Acid); EC 1.14.19.- (Fatty Acid Desaturases); EC 1.14.19.3 (FADS2 protein, mouse); JQS194YH3X (mead acid)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180122
[St] Status:MEDLINE

  4 / 30406 MEDLINE  
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[PMID]: 29353003
[Au] Autor:Qiu S; Zhang H; Fei Q; Zhu F; Wang J; Jia X; Chen B
[Ad] Address:Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Shi Zi Street No. 100, Hongshan Road, Jiangsu, Nanjing 210028, China; Key Laboratory of Chinese Medicine Delivery System of State Administration of Traditional Chinese Medicine, Jiangs
[Ti] Title:Urine and plasma metabolomics study on potential hepatoxic biomarkers identification in rats induced by Gynura segetum.
[So] Source:J Ethnopharmacol;216:37-46, 2018 Apr 24.
[Is] ISSN:1872-7573
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:ETHNOPHARMACOLOGICAL RELEVANCE: Gynura segetum (GS) is an herbal medicine containing Pyrrolizidine Alkaloids (PAs) that causes hepatic sinusoidal obstruction syndrome (HSOS). AIM OF THE STUDY: To discover potential biomarkers and metabolic mechanisms involved in the hepatotoxicity induced by GS. METHODS: SD rats were randomly divided into 4 groups including Saline, the decoction of GS high, medium and low dosage at dosages of 3.75g • kg , 7.5g • kg and 15g • kg . A metabolomics approach using Ultraperformance Liquid Chromatography -Quadrupole-Time-of-Flight / Mass Spectrometry (UPLC-Q-TOF/MS) was developed to perform the plasma and urinary metabolic profiling analysis, and identified differential metabolites by comparing the saline control group and decoction of GS groups. RESULTS: The herbal was presented dosage-dependent led to ingravescence of hepatotoxicity after the rats were consecutively given with the decoction of GS at varied dosages. A total of 18 differential metabolites of decoction of GS-induced hepatotoxicity were identified, while 10 of them including arginine, proline, glutamate, creatine, valine, linoleic acid, arachidonic acid, sphinganine, phytosphingosine, and citric acid could be discovered in urine and plasma, and primarily involved in Amino acid metabolism, Lipids metabolism and Energy metabolism. CONCLUSIONS: The results suggested that the differential metabolites of arginine, creatine, valine, glutamine and citric acid were verified as potential markers of GS-induced hepatotoxicity via the regulation of multiple metabolic pathways primarily involving in Amino acids metabolism and Energy metabolism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  5 / 30406 MEDLINE  
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[PMID]: 29518347
[Au] Autor:Lv Z; Fan H; Zhang B; Ning C; Xing K; Guo Y
[Ad] Address:State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing, China.
[Ti] Title:Dietary genistein supplementation in laying broiler breeder hens alters the development and metabolism of offspring embryos as revealed by hepatic transcriptome analysis.
[So] Source:FASEB J;:fj201701457R, 2018 Mar 08.
[Is] ISSN:1530-6860
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Genistein (GEN) is a type of isoflavone mainly derived from soy products. In this experiment, we added 40 and 400 mg/kg GEN to the diet of laying broiler breeder hens to clarify the maternal effects of GEN on the development and metabolism of chick embryos. GEN treatment at 40 mg/kg increased embryonic length, weight, and liver index, as well as the width of the proliferative zone in the tibial growth plate of chick embryos. Gene ontology (GO) cluster analysis of the hepatic transcriptome showed that GEN treatment promoted embryonic development and cell proliferation. Low-dose GEN treatment increased insulin growth factor-binding protein (IGFBP)3 mRNA expression in the embryonic liver, whereas high-dose GEN treatment increased IGFBP5 expression and activated the apoptosis and protein tyrosine kinase signaling pathways. Furthermore, adding supplemental GEN to the diet of hens promoted the glycolysis process in the embryonic liver through the insulin-signaling pathway, upregulated target genes (phosphoglucomutase-2, hexokinase 1, dihydroxyacetone phosphate by aldolase, phosphofructokinase, platelet, and enolase 2), and enhanced the transport of carboxylic acids and cholesterol and the synthesis of unsaturated fatty acid (arachidonic acid) in the embryonic liver through upregulation of liver X receptor, sterol regulatory element-binding protein 1, and patatin-like phospholipase A. Additionally, GEN treatment increased fatty acid -oxidation and Na /K -ATPase activity in the embryonic liver through activation of peroxisome proliferator-activated receptors (PPARs; PPARα and PPARδ) and the AMPK signaling pathway, which could provide energy for embryonic development. In addition, GEN treatment in hens increased superoxide dismutase activity and metallothionein expression in the chick embryonic liver and promoted lymphocyte proliferation through upregulation of mRNA expression of CDKN1A, IL12RB1, Sox11, PRKAR1A, PRKCQ, and TCF3. The improved immunity and antioxidant capacity, as a result of maternal GEN effects, was conducive to embryonic development. In conclusion, the addition of GEN to the diet of laying broiler breeder hens significantly promoted the development and metabolism of chick embryos.-Lv, Z., Fan, H., Zhang, B., Ning, C., Xing, K., Guo, Y. Dietary genistein supplementation in laying broiler breeder hens alters the development and metabolism of offspring embryos as revealed by hepatic transcriptome analysis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1096/fj.201701457R

  6 / 30406 MEDLINE  
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[PMID]: 29517182
[Au] Autor:Wendolowicz A; Stefanska E; Ostrowska L
[Ad] Address:Medical University of Bialystok, Department of Dietetics and Clinical Nutrition, Bialystok, Poland
[Ti] Title:Influence of selected dietary components on the functioning of the human nervous system
[So] Source:Rocz Panstw Zakl Hig;69(1):15-21, 2018.
[Is] ISSN:0035-7715
[Cp] Country of publication:Poland
[La] Language:eng
[Ab] Abstract:The diet is directly connected not only with the physical status but also with the functioning of the brain and the mental status. The potentially beneficial nutrients with a protective effect on the nervous system function include amino acids (tryptophan, phenylalanine, tyrosine, taurine), glucose and vitamins C, E, D and beta-carotene, B group vitamins (vitamin B12, vitamin B6, vitamin B4, vitamin B1) and minerals (selenium, zinc, magnesium, sodium, iron, copper, manganese, iodine). The presence of antioxidants in the diet protects against oxidative damage to nervous system cells. Biochemical data indicate that polyunsaturated fatty acids such as arachidonic acid (AA), docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA) and gamma-linolenic acid (GLA) as structural components of the nervous system play a key role in its function. The nutrition of the entire body also influences the production of neurotransmitters in the brain. A diet without an appropriate supply of protein, mineral nutrients or vitamins may result in a failure to form appropriately balanced numbers of neurotransmitters, which, as a result, may lead to neurotransmission dysfunction. This is the reason why proper nutrition is based on vegetables, fruits, whole-grain cereal products supplemented with products providing full-value protein (dairy products, fish, lean meat) and high-quality fat products (vegetable oils, fish fats).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

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[PMID]: 29423508
[Au] Autor:Lfqvist CA; Najm S; Hellgren G; Engstrm E; Svman K; Nilsson AK; Andersson MX; Hrd AL; Smith LEH; Hellstrm A
[Ad] Address:Section of Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gteborg, Sweden.
[Ti] Title:Association of Retinopathy of Prematurity With Low Levels of Arachidonic Acid: A Secondary Analysis of a Randomized Clinical Trial.
[So] Source:JAMA Ophthalmol;136(3):271-277, 2018 Mar 01.
[Is] ISSN:2168-6173
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Importance: Mice with oxygen-induced retinopathy fed matched diets except for ω-3 long-chain polyunsaturated fatty acids (LC-PUFAs) vs ω-6 LC-PUFAs demonstrate relative antiangiogenic and neuroprotective associations of ω-3 LC-PUFAs. However, supplementing preterm infants with LC-PUFAs has been inconsistent in reducing major preterm morbidities. However, few studies measured serum lipid levels after supplementation. Objective: To examine the associated risk of retinopathy of prematurity (ROP) from the levels of circulating ω-3 and ω-6 LC-PUFAs. Design, Setting, and Participants: This longitudinal clinical study was a further analysis of serum lipid levels from a randomized controlled trial cohort of 90 infants born at gestational age (GA) less than 28 weeks. From April 4, 2013, to September 22, 2015, cord blood samples, followed by venous blood samples, were obtained at birth and at 1, 7, 14, and 28 days after birth and then at postmenstrual age (PMA) 32, 36, and 40 weeks at the neonatal intensive care unit at Sahlgrenska University Hospital in Gteborg, Sweden. Main Outcomes and Measures: Serum phospholipid fatty acids were transmethylated and measured by gas chromatography-mass spectrometry. Mann-Whitney test, logistic regression Spearman rank correlation, and receiver operating characteristic curve analysis were used to compare differences between infants with no ROP and infants who developed ROP. Results: Serum levels from 78 infants (43 male [55%]; mean [SD] GA, 25.5 [1.4] weeks) with a known ROP outcome were evaluated. Lower area under the curve (AUC) of arachidonic acid (AA) (20:4 ω-6) was seen in infants with a later diagnosis of ROP compared with infants with no ROP in the first month of life (mean, 34.05 [95% CI, 32.10-36.00] vs 37.15 [95% CI, 34.85-39.46]; P < .05). In addition, lower levels of AA at 32 weeks' PMA were seen in infants with later severe ROP compared with in those without ROP (mean, 7.06 [95% CI, 6.60-7.52] vs 8.74 [95% CI, 7.80-9.67]; P < .001). In logistic modeling, low postnatal serum levels of AA and GA at birth identified with a sensitivity greater than 90% of infants who developed ROP. Conclusions and Relevance: Low postnatal levels of the ω-6 LC-PUFAs (AA) are strongly associated with ROP development. Evaluating postnatal AA fraction after birth in addition to GA may be useful for ROP prediction. Trial Registration: clinicaltrials.gov Identifier: NCT02760472.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Data-Review
[do] DOI:10.1001/jamaophthalmol.2017.6658

  8 / 30406 MEDLINE  
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[PMID]: 29326169
[Au] Autor:Goodman MC; Xu S; Rouzer CA; Banerjee S; Ghebreselasie K; Migliore M; Piomelli D; Marnett LJ
[Ad] Address:From the A. B. Hancock, Jr. Memorial Laboratory for Cancer Research, Departments of Biochemistry, Chemistry, and Pharmacology, Vanderbilt Institute of Chemical Biology and Center in Molecular Toxicology, Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee
[Ti] Title:Dual cyclooxygenase-fatty acid amide hydrolase inhibitor exploits novel binding interactions in the cyclooxygenase active site.
[So] Source:J Biol Chem;293(9):3028-3038, 2018 Mar 02.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The cyclooxygenases COX-1 and COX-2 oxygenate arachidonic acid (AA) to prostaglandin H (PGH ). COX-2 also oxygenates the endocannabinoids 2-arachidonoylglycerol (2-AG) and arachidonoylethanolamide (AEA) to the corresponding PGH analogs. Both enzymes are targets of nonsteroidal anti-inflammatory drugs (NSAIDs), but NSAID-mediated COX inhibition is associated with gastrointestinal toxicity. One potential strategy to counter this toxicity is to also inhibit fatty acid amide hydrolase (FAAH), which hydrolyzes bioactive fatty acid ethanolamides (FAEs) into fatty acids and ethanolamine. Here, we investigated the mechanism of COX inhibition by ARN2508, an NSAID that inhibits both COXs and FAAH with high potency, target selectivity, and decreased gastrointestinal toxicity in mouse models, presumably due to its ability to increase levels of FAEs. A 2.27--resolution X-ray crystal structure of the COX-2( )-ARN2508 complex reveals that ARN2508 adopts a binding pose similar to that of its parent NSAID flurbiprofen. However, ARN2508's alkyl tail is inserted deep into the top channel, an active site region not exploited by any previously reported NSAID. As for flurbiprofen, ARN2508's potency is highly dependent on the configuration of the α-methyl group. Thus, ( )-ARN2508 is more potent than ( )-ARN2508 for inhibition of AA oxygenation by both COXs and 2-AG oxygenation by COX-2. Also, similarly to ( )-flurbiprofen, ( )-ARN2508 exhibits substrate selectivity for inhibition of 2-AG oxygenation. Site-directed mutagenesis confirms the importance of insertion of the alkyl tail into the top channel for ( )-ARN2508's potency and suggests a role for Ser-530 as a determinant of the inhibitor's slow rate of inhibition compared with that of ( )-flurbiprofen.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.M117.802058

  9 / 30406 MEDLINE  
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[PMID]: 29298899
[Au] Autor:Edin ML; Hamedani BG; Gruzdev A; Graves JP; Lih FB; Arbes SJ; Singh R; Orjuela Leon AC; Bradbury JA; DeGraff LM; Hoopes SL; Arand M; Zeldin DC
[Ad] Address:From the Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, 27709 and.
[Ti] Title:Epoxide hydrolase 1 (EPHX1) hydrolyzes epoxyeicosanoids and impairs cardiac recovery after ischemia.
[So] Source:J Biol Chem;293(9):3281-3292, 2018 Mar 02.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Stimuli such as inflammation or hypoxia induce cytochrome P450 epoxygenase-mediated production of arachidonic acid-derived epoxyeicosatrienoic acids (EETs). EETs have cardioprotective, vasodilatory, angiogenic, anti-inflammatory, and analgesic effects, which are diminished by EET hydrolysis yielding biologically less active dihydroxyeicosatrienoic acids (DHETs). Previous assays have suggested that epoxide hydrolase 2 (EPHX2) is responsible for nearly all EET hydrolysis. EPHX1, which exhibits slow EET hydrolysis , is thought to contribute only marginally to EET hydrolysis. Using , , and mice, we show here that EPHX1 significantly contributes to EET hydrolysis Disruption of and/or genes did not induce compensatory changes in expression of other genes or family epoxygenases. Plasma levels of 8,9-, 11,12-, and 14,15-DHET were reduced by 38, 44, and 67% in mice compared with wildtype (WT) mice, respectively; however, plasma from mice exhibited significantly greater reduction (100, 99, and 96%) of those respective DHETs. Kinetic assays and FRET experiments indicated that EPHX1 is a slow EET scavenger, but hydrolyzes EETs in a coupled reaction with cytochrome P450 to limit basal EET levels. Moreover, we also found that EPHX1 activities are biologically relevant, as hearts had significantly better postischemic functional recovery (71%) than both WT (31%) and (51%) hearts. These findings indicate that mice are a valuable model for assessing EET-mediated effects, uncover a new paradigm for EET metabolism, and suggest that dual EPHX1 and EPHX2 inhibition may represent a therapeutic approach to manage human pathologies such as myocardial infarction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.RA117.000298

  10 / 30406 MEDLINE  
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[PMID]: 29515239
[Au] Autor:Virtanen JK; Mursu J; Voutilainen S; Tuomainen TP
[Ad] Address:University of Eastern Finland, Institute of Public Health and Clinical Nutrition, P.O. Box 1627, 70211, Kuopio, Finland. jyrki.virtanen@uef.fi.
[Ti] Title:The associations of serum n-6 polyunsaturated fatty acids with serum C-reactive protein in men: the Kuopio Ischaemic Heart Disease Risk Factor Study.
[So] Source:Eur J Clin Nutr;72(3):342-348, 2018 Mar.
[Is] ISSN:1476-5640
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND/OBJECTIVES: There are concerns that high intake of n-6 polyunsaturated fatty acids (PUFA) may promote inflammation, because the end-product of n-6 PUFA metabolism, arachidonic acid, is a precursor for pro-inflammatory eicosanoids. Our aim was to investigate cross-sectional associations of the serum n-6 PUFAs, objective biomarkers for exposure, with serum high-sensitivity C-reactive protein (CRP), a key inflammation marker. SUBJECTS/METHODS: The study included 1287 generally healthy men aged 42-60 years from the population-based Kuopio Ischaemic Heart Disease Risk Factor Study, examined in 1984-1989. ANCOVA and logistic regression were used for analyses. RESULTS: In the multivariable-adjusted analyses, both serum total n-6 PUFA and linoleic acid, the predominant n-6 PUFA, were associated with lower CRP. The mean CRP concentrations in quartiles of linoleic acid were 1.86, 1.51, 1.53, and 1.37 mg/L (P-trend = 0.001). The odds ratio for elevated CRP (>3 mg/L) in the highest vs. the lowest quartile was 0.47 (95% confidence interval (CI) 0.25-0.87, P-trend = 0.01). Arachidonic acid or the mainly endogenously produced n-6 PUFAs, gamma-linolenic acid and dihomo-gamma-linolenic acid, were not associated with higher CRP, either. Age, body mass index, or serum long-chain n-3 PUFA concentration did not modify the associations (P-interactions > 0.14). CONCLUSIONS: Serum n-6 PUFAs were not associated with increased inflammation in men. In contrast, the main n-6 PUFA linoleic acid had a strong inverse association with the key inflammation marker, CRP.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1038/s41430-017-0009-6


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