Samar I. Itani

TL;DR: The results indicated that the insulin resistance observed in human muscle when plasma FFA levels were elevated during euglycemic-hyperinsulinemic clamping was associated with increases in DAG mass and membrane-associated PKC-betaII and -delta and a decrease in IkappaB-alpha.

TL;DR: Both in vivo and in vitro, activation of AMPK was the first effect of gACRP30 and was transient, whereas alterations in malonyl CoA and ACC occurred later and were more sustained, indicating that gAC RP30 most likely exerts its actions on muscle fatty acid oxidation by inactivating ACC via activation ofAMPK and perhaps other signal transduction proteins.

TL;DR: The reported beneficial effects of exercise and metformin on cardiovascular disease and insulin resistance in humans could be related to the fact that they activate AMPK, which inhibits all of these events and enhances insulin signalling in the endothelial cell.

TL;DR: It is demonstrated that certain PKC inhibitors augment insulin-mediated glucose uptake and suggest that PKC may modulate insulin action in human skeletal muscle.

TL;DR: It is suggested that glucose autoregulates its own transport into skeletal muscle by a mechanism involving AMPK, and changes in whole-tissue concentrations of creatine phosphate ATP, or AMP, are left open, but they leave open the possibility that alterations in a cytosolic pool of these compounds play a regulatory role.