Visualization and quantitation of GLUT4 translocation in human skeletal muscle following glucose ingestion and exercise

Insulin- and contraction-stimulated increases in glucose uptake into skeletal<br />muscle occur in part as a result of the translocation of glucose transporter 4<br />(GLUT4) from intracellular stores to the plasma membrane (PM). This study<br />aimed to use immunofluorescence microscopy in human skeletal muscle to<br />quantify GLUT4 redistribution from intracellular stores to the PM in response<br />to glucose feeding and exercise. Percutaneous muscle biopsy samples were<br />taken from the m. vastus lateralis of ten insulin-sensitive men in the basal<br />state and following 30 min of cycling exercise (65% VO2 max). Muscle biopsy<br />samples were also taken from a second cohort of ten age-, BMI- and VO2 maxmatched insulin-sensitive men in the basal state and 30 and 60 min following<br />glucose feeding (75 g glucose). GLUT4 and dystrophin colocalization, measured<br />using the Pearson’s correlation coefficient, was increased following<br />30 min of cycling exercise (baseline r = 0.47 0.01; post exercise<br />r = 0.58 0.02; P < 0.001) and 30 min after glucose ingestion (baseline<br />r = 0.42 0.02; 30 min r = 0.46 0.02; P < 0.05). Large and small GLUT4<br />clusters were partially depleted following 30 min cycling exercise, but not<br />30 min after glucose feeding. This study has, for the first time, used immunofluorescence microscopy in human skeletal muscle to quantify increases in<br />GLUT4 and dystrophin colocalization and depletion of GLUT4 from large<br />and smaller clusters as evidence of net GLUT4 translocation to the PM.