Regulation of IRS-2 signaling by IGF-1 receptor in the diabetic rat heart

摘要: Cardiovascular disease involves changes in inflammatory markers. Since insulin/insulin-like growth factor 1 receptor (IGF-1R) can activate vascular endothelial to promote growth, reduced IGF-1R signaling the type I diabetic heart could be detrimental, leading reduced, collateral blood vessel growth. This study assessed whether diabetes induce an phenotype regulate molecules IGF-1 cascade, thus mediating apoptosis. Rats were made using streptozotocin (to render them diabetic) for 2 months with no insulin treatment. At months, rats sacrificed under anesthesia, and left ventricle was immediately removed placed into cold lysis buffer protein analyses. Western blotting, immunoprecipitation, enzyme-linked immunosorbent assay analyses completed evaluate levels. Diabetes increased TNF-alpha, interleukin-6 (IL-6), IL-1alpha levels heart. JNK p42/p44 activity significantly heart, while phosphorylation, IRS-2 tyrosine Akt activities reduced. A significant increase Bad cleavage of caspase 3 observed These results suggest that activates multiple markers which then signal a decrease key players insulin-signaling namely IGF-1R, IRS-2, Akt,