Glucose transport in adipocytes and its regulation by insulin.
Several lines of recent evidence indicate that in the absence of insulin glucose transport activity in the basal form of adipocytes is mostly associated with certain intracellular vesicles, and that the function of insulin is to translocate the glucose transport activity from the intracellular storage site to the plasma membrane. Upon sucrose density gradient centrifugation, the two subcellular structures associated with the glucose transport activity were fractionated into the plasma membrane-rich and Golgi-rich fractions. In our laboratory, the glucose transport activity in the subcellular fractions was assayed after reconstruction into egg lecithin liposomes. The apparent translocation of the glucose transport activity from the storage site to the plasma membrane was reversible, energy dependent, protein synthesis independent, almost completed in 5-10 min at 37 degrees C when the hormone concentration was 1 nM, and very slow at a low temperature (for example 15 degrees C). These results are consistent with the hypothesis that insulin regulates glucose transport activity in adipocytes by causing translocation of the glucose transport apparatus in a reversible manner, and that the translocation, or recycling, of the glucose transport apparatus is brought about by exo- and endocytosis.
D000273:Adipose Tissue / Q000166:cytology* / Q000187:drug effects; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002499:Centrifugation, Density Gradient; D005947:Glucose / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology*; D007700:Kinetics; D008081:Liposomes / Q000378:metabolism; D008297:Male; D008954:Models, Biological; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D051381:Rats; D013347:Subcellular Fractions / Q000378:metabolism
D007328:Insulin; D008081:Liposomes; D009004:Monosaccharide Transport Proteins; D005947:Glucose