Journal
CURRENT OPINION IN PHARMACOLOGY
Volume 9, Issue 6, Pages 753-762Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2009.07.004
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Funding
- INSERM
- CNRS
- University of Nice-Sophia Antipolis (France)
- ALFEDIAM-Abott Laboratory (France)
- European Commission (Brussels, Belgium) [LSHM-CT-2005-018734]
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Insulin receptor substrates (IRS) serine phosphorylation is a time-controlled physiological feedback mechanism in insulin signaling that is hijacked by metabolic and inflammatory stresses to promote insulin resistance. Kinases, including IKK beta, JNK, ERK, mTOR, and S6K, activated by the inducers of insulin resistance induce uncontrolled IRS serine phosphorylation. Studies with genetically modified mice reveal that these kinases integrate signals from metabolic and inflammatory stresses in adipose tissue, liver, and hypothalamus leading to peripheral and central insulin resistance. Moreover, IKK beta/NF-kappa B and JNK1 pathways in myeloid cells represent a core mechanism involved in inflammation linked to obesity. These kinases are thus potential drug targets against insulin resistance and the targeting of the IKK beta/NF-kappa B or the JNK pathway may evolve into future diabetes medication.
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