Aggressive Crosstalk Between Fatty Acids and Inflammation in Macrophages and Their Influence on Metabolic Homeostasis
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ORIGINAL PAPER
Aggressive Crosstalk Between Fatty Acids and Inflammation in Macrophages and Their Influence on Metabolic Homeostasis Kazuhiro Nishiyama1 · Yasuyuki Fujimoto1 · Tadayoshi Takeuchi1 · Yasu‑Taka Azuma1
Received: 27 February 2017 / Revised: 9 April 2017 / Accepted: 12 April 2017 © Springer Science+Business Media New York 2017
Abstract From the immunological point of view, macrophages are required to maintain metabolic homeostasis. Recently, there has been an increased focus on the influence of macrophage phenotypes in adipose tissue on the maintenance of metabolic homeostasis in healthy conditions because dysregulated metabolic homeostasis causes metabolic syndrome. This review notes several types of inflammatory and anti-inflammatory mediators in metabolic homeostasis. M1 macrophage polarization mediates inflammation, whereas M2 macrophage polarization mediates anti-inflammation. Fatty acids and their related factors mediate both inflammatory and anti-inflammatory responses. Saturated fatty acids and polyunsaturated fatty acids mediate inflammation, whereas marine-derived n-3 fatty acids, such as eicosapentaenoic acid and docosahexaenoic acid, mediate anti-inflammation. In this review, we discuss the current understanding of the crosstalk between fatty acids and inflammation in macrophages and their influence on metabolic homeostasis. Keywords Fatty acid · Macrophage · Inflammation · Anti-inflammation · Crosstalk · Metabolic disease
Introduction The maintenance of metabolic homeostasis in healthy life has been appreciated for a long time. Excessive * Yasu‑Taka Azuma [email protected]‑u.ac.jp 1
Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, 1‑58 Rinku‑ohraikita, Izumisano, Osaka 598‑8531, Japan
uncontrolled metabolic responses can result in a variety of metabolic diseases, including obesity and type 2 diabetes mellitus. Metabolic syndrome is defined as a distinct condition that increases the risk for cardiovascular disease, type 2 diabetes mellitus, fatty liver and cancer. The risk factors for metabolic syndrome also include dyslipidemia, hypertension, central obesity and insulin resistance [1–3]. The incidence of metabolic syndrome has increased around the world, including Japan, and it affects 30% of the US population and 25% of the European population [4–6]. Adipose tissue controls the body’s metabolism by producing several hormones and cytokines. Indeed, the strongest evidence supporting the influence of chronic inflammation in adipose tissue on the development of metabolic syndrome comes from large studies [4–6]. Inflammatory responses in adipose tissue in obesity may provide an understanding of the pathophysiological basis of metabolic syndrome. In adipose tissue in obesity, adipose cells become swollen, and inflammatory responses, including angiogenesis, deposition of extracellular matrix and macrophage infiltration, are significantly increased [7, 8]. Macrophages in adipose tissue r
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