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      Serum Polyunsaturated Fatty Acids Correlate with Serum Cytokines and Clinical Disease Activity in Crohn’s Disease

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          Abstract

          Crohn’s disease (CD) has been associated with an increased consumption of n-6 polyunsaturated fatty acid (PUFA), while greater intake of n-3 PUFA has been associated with a reduced risk. We sought to investigate serum fatty acid composition in CD, and associations of fatty acids with disease activity, cytokines, and adipokines. Serum was prospectively collected from 116 CD subjects and 27 non-IBD controls. Clinical disease activity was assessed by the Harvey Bradshaw Index (HBI). Serum fatty acids were measured by gas chromatography. Serum cytokines and adipokines were measured by Luminex assay. Dietary histories were obtained from a subset of patients. Nine serum cytokines and adipokines were increased in CD versus controls. CD subjects had increased percentage serum monounsaturated fatty acids (MUFA), dihomo-gamma linolenic acid (DGLA), eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and oleic acid, but decreased arachidonic acid (AA) versus controls. The % total n-3 fatty acids and % EPA directly correlated with pro-inflammatory cytokine levels and HBI, whereas the % total n-6 fatty acids were inversely correlated with pro-inflammatory cytokine levels and HBI. CD subjects had increased caloric intake versus controls, but no alterations in total fat or PUFA intake. We found differences in serum fatty acids, most notably PUFA, in CD that correlated both with clinical disease activity and inflammatory cytokines. Our findings indicate that altered fatty acid metabolism or utilization is present in CD and is related to disease activity.

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          Long-term intake of dietary fat and risk of ulcerative colitis and Crohn's disease.

          Dietary fats influence intestinal inflammation and regulate mucosal immunity. Data on the association between dietary fat and risk of Crohn's disease (CD) and ulcerative colitis (UC) are limited and conflicting.
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            Resolvins and protectins: mediating solutions to inflammation.

            Resolution of inflammation has historically been viewed as a passive process, occurring as a result of the withdrawal of pro-inflammatory signals, including lipid mediators such as leukotrienes and prostaglandins. Thus, most anti-inflammatory drugs have traditionally targeted primarily mediator pathways that are engaged at the onset of inflammation. Only recently has it been established that inflammation resolution is an active process with a distinct set of chemical mediators. Several clinical and epidemiological studies have identified beneficial effects of polyunsaturated fatty acids (PUFAs) for a variety of inflammatory diseases, yet without mechanistic explanations for these beneficial effects. Resolvins and protectins are recently identified molecules that are generated from omega-3 PUFA precursors and can orchestrate the timely resolution of inflammation in model systems. Dysregulation of pro-resolving mediators is associated with diseases of prolonged inflammation, so designing pharmacological mimetics of naturally occurring pro-resolving mediators offers exciting new targets for drug design. This review describes the discovery and synthesis of these novel lipid mediators, their receptors and mechanisms of action, and summarizes the studies to date that have uncovered roles for resolvins and protectins in disease states.
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              Alterations in lipid, amino acid, and energy metabolism distinguish Crohn’s disease from ulcerative colitis and control subjects by serum metabolomic profiling

              Introduction Biomarkers are needed in inflammatory bowel disease (IBD) to help define disease activity and identify underlying pathogenic mechanisms. We hypothesized that serum metabolomics, which produces unique metabolite profiles, can aid in this search. Objectives The aim of this study was to characterize serum metabolomic profiles in patients with IBD, and to assess for differences between patients with ulcerative colitis (UC), Crohn’s disease (CD), and non- IBD subjects. Methods Serum samples from 20 UC, 20 CD, and 20 non-IBD control subjects were obtained along with patient characteristics, including medication use and clinical disease activity. Non-targeted metabolomic profiling was performed using ultra-high performance liquid chromatography/mass spectrometry (UPLC-MS/MS) optimized for basic or acidic species and hydrophilic interaction liquid chromatography (HILIC/UPLC-MS/MS). Results In total, 671 metabolites were identified. Comparing IBD and control subjects revealed 173 significantly altered metabolites (27 increased and 146 decreased). The majority of the alterations occurred in lipid-, amino acid-, and energy-related metabolites. Comparing only CD and control subjects revealed 286 significantly altered metabolites (54 increased and 232 decreased), whereas comparing UC and control subjects revealed only 5 significantly altered metabolites (all decreased). Hierarchal clustering using significant metabolites separated CD from UC and control subjects. Conclusions We demonstrate that a number of lipid-, amino acid-, and tricarboxylic acid (TCA) cycle- related metabolites were significantly altered in IBD patients, more specifically in CD. Therefore, alterations in lipid and amino acid metabolism and energy homeostasis may play a key role in the pathogenesis of CD.
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                Author and article information

                Contributors
                lori.coburn@vumc.org
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                27 February 2019
                27 February 2019
                2019
                : 9
                : 2882
                Affiliations
                [1 ]ISNI 0000 0004 1936 9916, GRID grid.412807.8, Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, , Vanderbilt University Medical Center, ; Nashville, TN USA
                [2 ]ISNI 0000 0004 1936 9916, GRID grid.412807.8, Department of Pathology, , Microbiology, and Immunology, Vanderbilt University Medical Center, ; Nashville, TN USA
                [3 ]ISNI 0000 0004 1936 9916, GRID grid.412807.8, Vanderbilt Center for Mucosal Inflammation and Cancer, Department of Medicine, , Vanderbilt University Medical Center, ; Nashville, TN USA
                [4 ]ISNI 0000 0004 0420 4633, GRID grid.452900.a, Veterans Affairs Tennessee Valley Healthcare System, ; Nashville, TN USA
                [5 ]ISNI 0000 0004 1936 9916, GRID grid.412807.8, Vanderbilt Center for Stem Cell Biology, , Vanderbilt University Medical Center, ; Nashville, TN USA
                [6 ]ISNI 0000 0004 1936 9916, GRID grid.412807.8, Vanderbilt Ingram Cancer Center, , Vanderbilt University Medical Center, ; Nashville, TN USA
                Author information
                http://orcid.org/0000-0003-4421-1830
                Article
                39232
                10.1038/s41598-019-39232-z
                6393448
                30814550
                e5df65ed-1a2a-4076-abef-b1630d279099
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 12 October 2018
                : 18 January 2019
                Funding
                Funded by: FundRef https://doi.org/10.13039/100000062, U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases);
                Award ID: R01DK099204
                Award ID: P30DK058404
                Award ID: 5T32DK007673
                Award Recipient :
                Funded by: FundRef https://doi.org/10.13039/100000738, U.S. Department of Veterans Affairs (Department of Veterans Affairs);
                Award ID: I01BX001426
                Award ID: I01BX001453
                Award ID: 1IK2BX002126
                Award Recipient :
                Funded by: FundRef https://doi.org/10.13039/100000002, U.S. Department of Health & Human Services | National Institutes of Health (NIH);
                Award ID: R01AT004821
                Award ID: 3R01AT004821-02S1
                Award ID: R01DK053620
                Award ID: R01CA190612
                Award ID: P01CA028842
                Award ID: P01CA116087
                Award ID: UL1TR000445
                Award ID: DK20593
                Award Recipient :
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