» Articles » PMID: 28424949

Aggressive Crosstalk Between Fatty Acids and Inflammation in Macrophages and Their Influence on Metabolic Homeostasis

Overview
Journal Neurochem Res
Specialties Chemistry
Neurology
Date 2017 Apr 21
PMID 28424949
Citations 6
Authors
Affiliations
Soon will be listed here.
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.

Citing Articles

Systematisation of biological protectors for managing the metabolic syndrome development.

Benberin V, Sibagatova A, Nagimtayeva A, Akhmetova K, Voshchenkova T J Diabetes Metab Disord. 2021; 20(2):1449-1454.

PMID: 34900796 PMC: 8630288. DOI: 10.1007/s40200-021-00883-3.


Nutrigenomics of Dietary Lipids.

Bordoni L, Petracci I, Zhao F, Min W, Pierella E, Assmann T Antioxidants (Basel). 2021; 10(7).

PMID: 34206632 PMC: 8300813. DOI: 10.3390/antiox10070994.


Changes in peripheral blood compounds following psychopharmacological treatment in drug-naïve first-episode patients with either schizophrenia or major depressive disorder: a meta-analysis.

Cakici N, Sutterland A, Penninx B, de Haan L, van Beveren N Psychol Med. 2021; 51(4):538-549.

PMID: 33653423 PMC: 8020491. DOI: 10.1017/S0033291721000155.


Pattern Recognition Receptor-Mediated Chronic Inflammation in the Development and Progression of Obesity-Related Metabolic Diseases.

Yu L, Li Y, Du C, Zhao W, Zhang H, Yang Y Mediators Inflamm. 2019; 2019:5271295.

PMID: 31582899 PMC: 6754942. DOI: 10.1155/2019/5271295.


Acute high-fat feeding leads to disruptions in glucose homeostasis and worsens stroke outcome.

Haley M, Krishnan S, Burrows D, de Hoog L, Thakrar J, Schiessl I J Cereb Blood Flow Metab. 2017; 39(6):1026-1037.

PMID: 29171775 PMC: 6545621. DOI: 10.1177/0271678X17744718.


References
1.
Talukdar S, Olefsky J, Osborn O . Targeting GPR120 and other fatty acid-sensing GPCRs ameliorates insulin resistance and inflammatory diseases. Trends Pharmacol Sci. 2011; 32(9):543-50. PMC: 3419590. DOI: 10.1016/j.tips.2011.04.004. View

2.
Li Y, Yan H, Zhang Z, Zhang G, Sun Y, Yu P . Andrographolide derivative AL-1 improves insulin resistance through down-regulation of NF-κB signalling pathway. Br J Pharmacol. 2015; 172(12):3151-8. PMC: 4459030. DOI: 10.1111/bph.13118. View

3.
Henao-Mejia J, Elinav E, Jin C, Hao L, Mehal W, Strowig T . Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity. Nature. 2012; 482(7384):179-85. PMC: 3276682. DOI: 10.1038/nature10809. View

4.
Furuhashi M, Hotamisligil G . Fatty acid-binding proteins: role in metabolic diseases and potential as drug targets. Nat Rev Drug Discov. 2008; 7(6):489-503. PMC: 2821027. DOI: 10.1038/nrd2589. View

5.
Han M, Jung D, Morel C, Lakhani S, Kim J, Flavell R . JNK expression by macrophages promotes obesity-induced insulin resistance and inflammation. Science. 2012; 339(6116):218-22. PMC: 3835653. DOI: 10.1126/science.1227568. View