Translocation hypothesis of insulin action on glucose transport.
This article reviews the experimental data that support the translocation hypothesis of insulin action on glucose transport in adipocytes. According to this hypothesis, 1) most of the glucose transport mechanism in the basal (no insulin) form of fat cells is associated with an unidentified subcellular structure (the storage site), which is separated into the Golgi-rich fraction by centrifugation, and 2) the function of insulin is to induce translocation of the glucose transport mechanism from the above storage site to the plasma membrane. This translocation of the transport mechanism is reversible, dependent on metabolic energy, and independent of protein synthesis.
D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism*; D002474:Cell-Free System; D005947:Glucose / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology*; D007425:Intracellular Membranes / Q000187:drug effects / Q000378:metabolism*; D009004:Monosaccharide Transport Proteins
D002352:Carrier Proteins; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D005947:Glucose