AKT1 and Insulin resistance: Namely, the literature [8,49] indicates alterations in the insulin-signaling pathway (decreased tyrosine phosphorylation and increased serine phosphorylation of the insulin receptor), and disturbances of the intracellular insulin pathway (reduced Akt/PKB and AS160 phosphorylation and activation in muscle cells, which impair insulin-stimulated glucose uptake and therefore contribute to insulin resistance).