The potential of AMPK to stimulateGLUT4 translocation to matlab plasma membrane in skeletal muscle is by engineering alternative mechanismthan that motivated by insulin and insulin and AMPK consequences are additive. Under ischemic/hypoxic circumstances in matlab middle matlab activation of AMPK leads to thephosphorylation and activation engineering matlab kinase activity of phosphofructokinase 2, PFK 26 phosphofructo 2 kinase. The product engineering matlab motion of PFK 2 fructose 2,6 bisphosphate,F2,6BP is one engineering matlab most mighty regulators engineering matlab rate of flux throughglycolysis and gluconeogenesis. In liver matlab PKA mediated phosphorylation of PFK 2 effects in conversion of theenzyme from engineering kinase that generates F2,6BP to engineering phosphatase that removes the2 phosphate thus lowering matlab degrees engineering matlab powerful allosteric activator engineering matlab glycolyticenzyme 6 phosphfructo 1 kinase, PFK 1 and matlab strong allosteric inhibitorof matlab gluconeogenic enzyme fructose 1,6 bisphosphatase F1, 6BPase. It is essential to notice that like many enzymes, there are varied isoforms of PFK 2at least 4 and neither matlab liver or matlab skeletal muscle isoforms include matlab AMPKphosphorylation websites found in matlab cardiac and inducible iPFK2 isoforms of PFK 2. Inducible PFK 2 is expressed in matlab monocyte/macrophage lineage in line with pro inflammatory stimuli.