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Up-regulation of liver system A for neutral amino acid transport in euglycemic hyperinsulinemic rats
A Ferrer-Martínez1, J Casado, A Leturque
1Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Spain.
To determine the role of insulin on the in vivo modulation of liver system A activity, we used the euglycemic hyperinsulinemic clamp coupled to the measurement of solute uptakes into plasma membrane vesicles partially purified from livers of hyperinsulinemic rats and their saline-infused controls. The clamp was performed in chronically catheterized rats, either in the fasted state, 24 h after surgery (Group I), or after 3 days of recovery (Group II). System A activity, measured as the MeAIB-inhibitable L-alanine uptake, was selectively induced by hyperinsulinemia, although the effect was much greater in Group II than in Group I rats (137% vs. 24% over the basal values, respectively). This might be explained by the higher basal levels found in those liver plasma membrane vesicles from Group I fasted animals. Hyperinsulinemia also decreased blood amino acids but to a similar extent in both experimental groups. This suggests that amino acid depletion by itself may not cause up-regulation of system A. Other transport activities involved in neutral amino acid transport (Systems ASC, N and L) were not modified by the clamp. The induction of system A cannot be explained by changes in the dissipation rate of the Na+ transmembrane gradient, because the differences between insulin- and saline-infused rats remained even when the electrochemical Na+ gradient was disrupted in the presence of monensin. Thus, hyperinsulinemia might induce an increase in the number of transporters inserted into the plasma membrane.
To determine the role of insulin on the in vivo modulation of liver system A activity, we used the euglycemic hyperinsulinemic clamp coupled to the measurement of solute uptakes into plasma membrane vesicles partially purified from livers of hyperinsulinemic rats and their saline-infused controls. The clamp was performed in chronically catheterized rats, either in the fasted state, 24 h after surgery (Group I), or after 3 days of recovery (Group II). System A activity, measured as the MeAIB-inhibitable L-alanine uptake, was selectively induced by hyperinsulinemia, although the effect was much greater in Group II than in Group I rats (137% vs. 24% over the basal values, respectively). This might be explained by the higher basal levels found in those liver plasma membrane vesicles from Group I fasted animals. Hyperinsulinemia also decreased blood amino acids but to a similar extent in both experimental groups. This suggests that amino acid depletion by itself may not cause up-regulation of system A. Other transport activities involved in neutral amino acid transport (Systems ASC, N and L) were not modified by the clamp. The induction of system A cannot be explained by changes in the dissipation rate of the Na+ transmembrane gradient, because the differences between insulin- and saline-infused rats remained even when the electrochemical Na+ gradient was disrupted in the presence of monensin. Thus, hyperinsulinemia might induce an increase in the number of transporters inserted into the plasma membrane.