Insulin is known to increase the number of cell surface insulin-like growth factor II (IGF-II) receptors in isolated rat adipose cells through a subcellular redistribution mechanism similar to that for the glucose transporter. The effects of insulin on these two processes, therefore, have now been directly compared in the same cell preparations. 1) Insulin increases the steady state number of cell surface IGF-II receptors by 7-13-fold without affecting receptor affinity; however, insulin stimulates glucose transport activity by 25-40-fold. 2) The insulin concentration required for half-maximal stimulation of cell surface IGF-II receptor number is ~30% lower than that for the stimulation of glucose transport activity. 3) The half-time for the achievement of insulin's maximal effect at 37°C is much shorter for IGF-II receptor number (~0.8 min) than for glucose transport activity (~2.6 min). 4) Reversal of insulin's action at 37°C occurs more rapidly for cell surface IGF-II receptors (t( 1/2 ) ≃ 2.9 min) than for glucose transport activity (t( 1/2 ) ≃ 4.9 min). 5) When the relative subcellular distribution of IGF-II receptors is examined in basal cells, < 10% of the receptors are localized to the plasma membrane fraction indicating that most of the receptors, like glucose transporters, are localized to an intracellular compartment. However, in response to insulin, the number of plasma membrane IGF-II receptors increases only ~1.4-fold while the number of glucose transporters increases ~4.5-fold. Thus, while the stimulatory actions of insulin on cell surface IGF-II receptors and glucose transport activity are qualitatively similar, marked quantitative differences suggest that the subcellular cycling of these two integral membrane proteins occurs by distinct processes.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Biological Chemistry|
|State||Published - Jan 1 1988|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology