Inhibition of insulin signalling by the c-Jun N terminal kinase (JNK) pathway: Output on systemic insulin resistance
Speaker: Carme Caelles
Facultad de Farmacia; Universidad de Barcelona [Barcelona, Spain]
Host: Faustino Mollinedo
Salón de Actos del CICInhibition of insulin signalling by the c-Jun N terminal kinase (JNK) pathway: Output on systemic insulin resistance
Insulin resistance is a defective response to insulin in target tissues and is proposed to increase insulin demand. Consequently, it induces hyperinsulinemia and finally, the pancreatic failure that leads to hyperglycemia, characteristic conditions of type 2 diabetes. At molecular level, insulin resistance is induced by different mechanisms, being the insulin receptor substrate (IRS) phosphorylation on serine residues one of the most relevant. Among several protein kinases, the c-Jun N-terminal kinase (JNK) kinase plays a major role in IRS-1/2 serine phosphorylation, and therefore, inhibits insulin signalling in different target tissues. Results related to the regulation of the JNK activity in different insulin target tissues, and its consequences on systemic versus tissue-specific insulin resistance will be discussed.