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      Arachidonic Acid Metabolites in Cardiovascular and Metabolic Diseases

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          Abstract

          Lipid and immune pathways are crucial in the pathophysiology of metabolic and cardiovascular disease. Arachidonic acid (AA) and its derivatives link nutrient metabolism to immunity and inflammation, thus holding a key role in the emergence and progression of frequent diseases such as obesity, diabetes, non-alcoholic fatty liver disease, and cardiovascular disease. We herein present a synopsis of AA metabolism in human health, tissue homeostasis, and immunity, and explore the role of the AA metabolome in diverse pathophysiological conditions and diseases.

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          Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs.

          J R Vane (1971)
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            Anti-inflammatory therapy in chronic disease: challenges and opportunities.

            Ira Tabas, Christopher K. Glass (2013)
            A number of widespread and devastating chronic diseases, including atherosclerosis, type 2 diabetes, and Alzheimer's disease, have a pathophysiologically important inflammatory component. In these diseases, the precise identity of the inflammatory stimulus is often unknown and, if known, is difficult to remove. Thus, there is interest in therapeutically targeting the inflammatory response. Although there has been success with anti-inflammatory therapy in chronic diseases triggered by primary inflammation dysregulation or autoimmunity, there are considerable limitations. In particular, the inflammatory response is critical for survival. As a result, redundancy, compensatory pathways, and necessity narrow the risk:benefit ratio of anti-inflammatory drugs. However, new advances in understanding inflammatory signaling and its links to resolution pathways, together with new drug development, offer promise in this area of translational biomedical research.
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              Insulin sensitivity: modulation by nutrients and inflammation.

              Simon Schenk, Maziyar Saberi, Jerrold Olefsky (2008)
              Insulin resistance is a major metabolic feature of obesity and is a key factor in the etiology of a number of diseases, including type 2 diabetes. In this review, we discuss potential mechanisms by which brief nutrient excess and obesity lead to insulin resistance and propose that these mechanisms of action are different but interrelated. We discuss how pathways that "sense" nutrients within skeletal muscle are readily able to regulate insulin action. We then discuss how obesity leads to insulin resistance via a complex interplay among systemic fatty acid excess, microhypoxia in adipose tissue, ER stress, and inflammation. In particular, we focus on the hypothesis that the macrophage is an important cell type in the propagation of inflammation and induction of insulin resistance in obesity. Overall, we provide our integrative perspective regarding how nutrients and obesity interact to regulate insulin sensitivity.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 23 October 2018
                Publication date Collection: November 2018
                Volume: 19
                Issue: 11
                Electronic Location Identifier: 3285
                Affiliations
                Department of Internal Medicine II, Medical University Innsbruck, Innsbruck 6020, Austria; Thomas.Sonnweber@ 123456i-med.ac.at (T.S.); Alex.Pizzini@ 123456i-med.ac.at (A.P.); Manfred.Nairz@ 123456i-med.ac.at (M.N.); guenter.weiss@ 123456i-med.ac.at (G.W.)
                Author notes
                [* ]Correspondence: Ivan.Tancevski@ 123456i-med.ac.at ; Tel.: +43-512-504-81602
                Author information
                https://orcid.org/0000-0002-5080-386X
                https://orcid.org/0000-0003-0709-2158
                Article
                Publisher ID: ijms-19-03285
                DOI: 10.3390/ijms19113285
                PMC ID: 6274989
                PubMed ID: 30360467
                SO-VID: bd2ffcf3-74e5-4b02-a5d1-c74e967b9467
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 30 September 2018
                Date accepted : 21 October 2018
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: arachidonic acid,eicosanoids,metabolic disease,obesity,nonalcoholic fatty liver disease,diabetes,atherosclerosis,cardiovascular disease,cholesterol
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: arachidonic acid, eicosanoids, metabolic disease, obesity, nonalcoholic fatty liver disease, diabetes, atherosclerosis, cardiovascular disease, cholesterol

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