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Mediators of Inflammation
Volume 2010 (2010), Article ID 359732, 18 pages
Review Article

Role of Heme Oxygenase in Inflammation, Insulin-Signalling, Diabetes and Obesity

Department of Physiology, College of Medicine, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK, Canada S7N 5E5

Received 12 December 2009; Revised 15 February 2010; Accepted 24 February 2010

Academic Editor: Giuseppe Matarese

Copyright © 2010 Joseph Fomusi Ndisang. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Diabetes and obesity are chronic conditions associated with elevated oxidative/inflammatory activities with a continuum of tissue insults leading to more severe cardiometabolic and renal complications including myocardial infarction and end-stage-renal damage. A common denominator of these chronic conditions is the enhanced the levels of cytokines like tumour necrosis factor-alpha (TNF- 𝛼 ), interleukin (IL-6), IL-1 𝛽 and resistin, which in turn activates the c-Jun-N-terminal kinase (JNK) and NF- 𝜅 B pathways, creating a vicious cycle that exacerbates insulin resistance, type-2 diabetes and related complications. Emerging evidence indicates that heme oxygenase (HO) inducers are endowed with potent anti-diabetic and insulin sensitizing effects besides their ability to suppress immune/inflammatory response. Importantly, the HO system abates inflammation through several mechanisms including the suppression of macrophage-infiltration and abrogation of oxidative/inflammatory transcription factors like NF- 𝜅 B, JNK and activating protein-1. This review highlights the mechanisms by which the HO system potentiates insulin signalling, with particular emphasis on HO-mediated suppression of oxidative and inflammatory insults. The HO system could be explored in the search for novel remedies against cardiometabolic diseases and their complications.