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Role of heme oxygenase in inflammation, insulin-signalling, diabetes and obesity Ndisang JFMediators Inflamm 2010[]; 2010 (ä): 359732Diabetes 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-alpha), interleukin (IL-6), IL-1beta and resistin, which in turn activates the c-Jun-N-terminal kinase (JNK) and NF-kappaB 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-kappaB, 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.|*Signal Transduction[MESH]|Animals[MESH]|Diabetes Mellitus, Type 2/complications/*metabolism/physiopathology[MESH]|Heme Oxygenase (Decyclizing)/*metabolism[MESH]|Humans[MESH]|Inflammation/*metabolism[MESH]|Insulin Resistance/physiology[MESH]|Insulin/*metabolism[MESH]|Isoenzymes/*metabolism[MESH]|NF-kappa B/metabolism[MESH]|Obesity/complications/*metabolism/physiopathology[MESH]|Oxidative Stress[MESH] |
