Minireviews
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
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
Abstract

In obesity, persistent low-grade inflammation is considered as a major contributor towards the progression to insulin resistance and type 2 diabetes while in lean subjects the immune environment is non-inflammatory. Massive adipose tissue (AT) infiltration by pro-inflammatory M1 macrophages and several T cell subsets as obesity develops leads to the accumulation - both in the AT and systemically - of numerous pro-inflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor α, IL-17 and IL-6 which are strongly associated with the progression of the obese phenotype towards the metabolic syndrome. At the same time, anti-inflammatory M2 macrophages and Th subsets producing the anti-inflammatory cytokines IL-10, IL-5 and interferon-γ, including Th2 and T-reg cells are correlated to the maintenance of AT homeostasis in lean individuals. Here, we discuss the basic principles in the control of the interaction between the AT and infiltrating immune cells both in the lean and the obese condition with a special emphasis on the contribution of pro- and anti-inflammatory cytokines to the establishment of the insulin-resistant state. In this context, we will discuss the current knowledge about alterations in the levels on pro- and anti-inflammatory cytokines in obesity, insulin resistance and type 2 diabetes mellitus, in humans and animal models. Finally, we also briefly survey the recent novel therapeutic strategies that attempt to alleviate or reverse insulin resistance and type 2 diabetes via the administration of recombinant inhibitory antibodies directed towards some pro-inflammatory cytokines.

Keywords: Type 2 diabetes, Crown-like structures, Adipose tissue inflammation, Macrophages, Eosinophils, Obesity

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.