(11-02-08) Inflammatory mechanisms in the regulation of insulin resistance.

Tilg H, Moschen AR.

Christian Doppler Research Laboratory for Gut Inflammation and Department of Gastroenterology and Hepatology, Innsbruck Medical University, Innsbruck, Austria.

Insulin resistance (IR) plays a key role in the pathophysiology of obesity-related diseases such as type 2 diabetes and non-alcoholic fatty liver disease. It has been demonstrated that IR is associated with a state of chronic low-grade inflammation and several mediators released from various cell types including immune cells and adipocytes have been identified being involved in the development of IR. Amongst those are several pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin (IL) -1, IL-6, and various adipocytokines. Furthermore, several transcription factors and kinases such as c-Jun N-terminal kinase (JNK) and inhibitor of kappa B kinase -beta (IKKbeta), a kinase located proximal of nuclear factor -kappaB (NF-kappaB) participate in this process. Hepatocyte-specific overexpression of NF-kappaB is associated with IR and can mimic all features of fatty liver disease. Whereas the evidence for an important role of many pro-inflammatory pathways in IR in in vitro and animal studies is overwhelmingly, data from interventional studies in humans to prove this concept are still minor. As a complex network of inflammatory cytokines, adipocytokines, transcription factors, receptor molecules and acute phase reactants are involved in the development of IR, new therapeutic approaches in IR-related diseases will be based on a better understanding of their complex interactions.

Source: Mol Med. 2008 Jan 31

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