Phosphorylation of p38 MAPK and cytosolic phospholipase A<sub>2</sub> (cPLA<sub>2</sub>) was enhanced after incubation of platelets with T2D TGRL and thrombin (+87% and +32%, respectively, P < 0.05) compared with platelets incubated with thrombin only.
Our data demonstrate a novel role of NOS1AP in regulating hepatic insulin sensitivity and p38 MAPK inactivation in obese mice, which makes NOS1AP a potential therapeutic target for the prevention and treatment of T2D.
In addition, type 2 diabetes mellitus promoted a more aggressive phenotype associated with up-regulated p38 MAPK activity, which was effectively inhibited by VCP979.
In the present study, adult male C57BL/6J mice with streptozotocin (STZ)-induced T2DM mice were subjected to photothrombotic ischemic stroke and treatment with p38 MAPK inhibitors.
Our results indicated the considerably aberrant MAPK signaling in both insulin-sensitive tissues of T2D rat, and that the p38 may play a role as a common "hub" in the gene module response to hyperglycaemia.
Hence, our results define a crucial role for phosphorylation on Thr48 and Ser61 of Xbp1s in the maintenance of glucose homeostasis in obesity, and they suggest that p38 MAPK activation in the livers of obese mice could lead to a new therapeutic approach to the treatment of type 2 diabetes.