A Molecular and Whole Body Insight of the Mechanisms Surrounding Glucose Disposal and Insulin Resistance with Hypoxic Treatment in Skeletal Muscle

Figure 1

Insulin and contraction signaling pathways during GLUT-4 recruitment and translocation. Adapted from Mackenzie and Elliott [60]. IRS, insulin receptor substrate; PI3-K, class IA phosphatidylinositol 3-kinase; PIP2, phosphatidylinositol 4,5-bisphosphate; PIP3, phosphatidylinositol 3,4,5-trisphosphate; PDK1, phosphoinositide-dependent protein kinase-1; Akt, serine/threonine protein kinase; AS160, 160 kDa Akt substrate; GLUT-4, glucose transporter 4; GSV, GLUT-4 storage vesicle; Rab-GAP, Rab-GTPase-activating protein; Rab-GDP, guanosine-50-diphosphate-loaded Rab; Rab-GTP, guanosine-50-triphosphate-loaded Rab; CaMKK, Ca²⁺/calmodulin-dependent protein kinase kinase; LKB1, serine/threonine kinase 11; STRAD, putative kinase; MO25, mouse protein 25/scaffold protein; AMPK, 5′-monophosphate-activated protein kinase; Thr¹⁷², phosphorylated AMPKα at threonine 172; AMP, adenosine monophosphate; ATP, adenosine triphosphate; P, phosphorylated site.