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Regulation of glucose transport by cyclic amp stimulators via 3 different mechanisms in rat and human adipocytes

, : Regulation of glucose transport by cyclic amp stimulators via 3 different mechanisms in rat and human adipocytes. Journal of Biological Chemistry 258(22): 13685-13692

The regulation of glucose transport by a .beta.-adrenergic agonist and other cAMP stimulators was assessed by kinetic analyses of 3-O-methylglucose (MG) transport in rat and human adipocytes and in isolated rat plasma membrane vesicles. Basal MG transport was biphasically affected by L-isoproterenol in rat adipocytes: lower concentrations (10-25 nM) of L-isoproterenol stimulated the basal rate by increasing the Vmax, but higher concentrations (0.5-2 .mu.M) of L-isoproterenol inhibited the basal rate. On the other hand, the maximum insulin-stimulated MG transport rate was not affected by 25 nM L-isoproterenol, but was suppressed by 2 .mu.M L-isoproterenol in rat adipocytes. In the presence of adenosine deaminase plus L-isoproterenol (25 nM and 2 .mu.M), dibutyryl AMP (Bt2cAMP), 3-isobutyl-1-methylxanthine, or forskolin, both basal and the maximum rates of MG transport were suppressed in rat adipocytes. However, from kinetic experiments, both L-isoproterenol plus adenosine deaminase and Bt2cAMP decreased the Vmax. On the other hand, isobutymethylxanthine and forskolin decreased the Vmax as well as increased the Ks. MG transport in plasma membrane vesicles was directly inhibited by either forskolin or isobutyl-methylxanthine. In contrast, both 25 nM and 2 .mu.M L-isoproterenol with or without adenosine deaminase, Bt2cAMP or cAMP had no effect on MG transport in rat plasma membrane vesicles. In human adipocytes, L-isoproterenol always stimulated basal MG transport and did not suppress the maximum rate of MG transport, even though cAMP production was maximally stimulated by L-isoproterenol. Both adenosine deaminase plus L-isoproterenol and Bt2cAMP did not suppress the basal rate, but did show a modest suppression (40%) of the maximum insulin effect on MG transport in human adipocytes. However, both isobutylmethylxanthine and forskolin remarkably suppressed (85%) both the basal and the maximum rate of MG transport by both increasing the Ks and decreasing the Vmax. MG transport was indicated in both rat and human adipocytes is regulated by 3 different mechanisms: L-isoproterenol, a .beta.-adrenergic agonist, stimulates basal MG transport by increasing the Vmax, cAMP mediates a decrease in MG transport by decreasing the Vmax, and both forskolin and isobutylmethylxanthine also decrease MG transport by directly inhibiting the binding of MG molecules to transporters, resulting in a decrease in the Vmax and an increase in the Ks.

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