Pirola L, Ferraz JC. Role of pro- and anti-inflammatory phenomena in the physiopathology of type 2 diabetes and obesity. World J Biol Chem 2017; 8(2): 120-128 [PMID: 28588755 DOI: 10.4331/wjbc.v8.i2.120]
Corresponding Author of This Article
Dr. Luciano Pirola, INSERM Unit 1060, South Lyon Hospital, Medical Faculty, 165 Ch. du Grand Revoyet - BP12, 69921 Oullins, France. luciano.pirola@univ-lyon1.fr
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Biol Chem. May 26, 2017; 8(2): 120-128 Published online May 26, 2017. doi: 10.4331/wjbc.v8.i2.120
Role of pro- and anti-inflammatory phenomena in the physiopathology of type 2 diabetes and obesity
Luciano Pirola, José Candido Ferraz
Luciano Pirola, José Candido Ferraz, INSERM Unit 1060, South Lyon Hospital, Medical Faculty, 69921 Oullins, France
José Candido Ferraz, Academic Center of Vitoria, Federal University of Pernambuco, Pernambuco 55608-680, Brazil
Author contributions: Both authors contributed equally to this paper.
Supported by The Franco-Brazilian CAPES/COFECUB collaboration program Me797-14. Ferraz JC was supported by a CAPES postdoctoral fellowship.
Conflict-of-interest statement: Neither author has conflicts of interest to declare.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Luciano Pirola, INSERM Unit 1060, South Lyon Hospital, Medical Faculty, 165 Ch. du Grand Revoyet - BP12, 69921 Oullins, France. luciano.pirola@univ-lyon1.fr
Telephone: +33-4-26235948
Received: November 25, 2016 Peer-review started: November 29, 2016 First decision: January 16, 2017 Revised: January 24, 2017 Accepted: February 18, 2017 Article in press: February 19, 2017 Published online: May 26, 2017 Processing time: 173 Days and 5.8 Hours
Core Tip
Core tip: Low-grade inflammation of adipose tissue (AT) contributes to insulin resistance and type 2 diabetes in obese patients. On the contrary, in lean individuals, the immune environment of AT is non-inflammatory. In obesity, AT is infiltrated by pro-inflammatory macrophages and T cells leading to the accumulation of interleukin-1β (IL-1β), tumor necrosis factor α, IL-17 and IL-6. On the contrary, M2 macrophages, Th2 and T-regs cells producing anti-inflammatory IL-10, IL-5 and interferon-γ, are present in AT of lean individuals. Here, we discuss the interaction between AT and infiltrating immune cells in the lean vs the obese condition, with emphasis on the contribution of pro- and anti-inflammatory cytokines to the establishment of insulin resistance.
