| pubmed-article:18056775 | pubmed:abstractText | Elevated plasma free fatty acids, excess reactive oxygen species, inflammation, and gluco-counterregulatory hormones induce insulin resistance (IR) through activation of Jun NH(2)-terminal kinase and nuclear factor-kappaB inhibitor kappaB kinase, which leads to hyperphosphorylation of the insulin receptor substrate type 1. Aspirin blocks nuclear factor-kappaB inhibitor kappaB kinase and improves IR in type 2 diabetes mellitus. | lld:pubmed |
