Insulin promotes potassium uptake into skeletal muscle by stimulating the activity of the Na+-K+ pump. To test whether insulin-induced glucose and potassium uptake are linked processes in vivo, we used the perfused forearm technique in healthy volunteers. Local hyperinsulinemia (125 ± 11 μU/ml for 100 min) induced a net uptake of glucose and potassium (4.79 ± 0.62 and 0.76± 0.22 μmol·min-1·100 ml-1 of forearm volume, respectively). When an intra-arterial ouabain infusion (0.72 μg·min-1·100 ml-1, producing local levels of ~0.5 mM) was superimposed on the insulin infusion, potassium uptake was blocked (0.026 ± 0.190 ml·min-1·100 ml-1, P < 0.02), and glucose uptake was decreased (to 3.31 ± 0.34 μmol·min-1·100 ml-1, P < 0.03). The latter change was explained by a 30% fall in forearm blood flow (from 2.95 ± 0.01 to 2.01 ± 0.18 ml·min-1·100 ml-1, P < 0.001). To separate out the effect of blood flow, in another series of studies forearm blood flow was clampted by co-infusing propranolol and phentolamine (7 and 8 μg·min-1·min-1, respectively). Under these conditions of fixed flow (7.0 ± 0.8 ml·min-1·100 ml-1), ouabain still abolished the stimulatory effect of insulin on potassium uptake but had only a small (and statistically insignificant) effect on forearm glucose extraction (from 20 ± 2 to 16 ± 2%, P = NS). We conclude that in human forearm muscle ouabain inhibits Na+-K+ exchange and depresses insulin-induced glucose uptake via an adrenergic-mediated limitation of blood flow. When vasoconstriction is prevented, the actions of insulin on glucose and potassium influx appear to be largely independent of one another.
Independent stimulation of glucose metabolism and Na+-K+ exchange by insulin in the human forearm.
FERRANNINI, ELEUTERIO;TADDEI, STEFANO;NATALI, ANDREA;
1988-01-01
Abstract
Insulin promotes potassium uptake into skeletal muscle by stimulating the activity of the Na+-K+ pump. To test whether insulin-induced glucose and potassium uptake are linked processes in vivo, we used the perfused forearm technique in healthy volunteers. Local hyperinsulinemia (125 ± 11 μU/ml for 100 min) induced a net uptake of glucose and potassium (4.79 ± 0.62 and 0.76± 0.22 μmol·min-1·100 ml-1 of forearm volume, respectively). When an intra-arterial ouabain infusion (0.72 μg·min-1·100 ml-1, producing local levels of ~0.5 mM) was superimposed on the insulin infusion, potassium uptake was blocked (0.026 ± 0.190 ml·min-1·100 ml-1, P < 0.02), and glucose uptake was decreased (to 3.31 ± 0.34 μmol·min-1·100 ml-1, P < 0.03). The latter change was explained by a 30% fall in forearm blood flow (from 2.95 ± 0.01 to 2.01 ± 0.18 ml·min-1·100 ml-1, P < 0.001). To separate out the effect of blood flow, in another series of studies forearm blood flow was clampted by co-infusing propranolol and phentolamine (7 and 8 μg·min-1·min-1, respectively). Under these conditions of fixed flow (7.0 ± 0.8 ml·min-1·100 ml-1), ouabain still abolished the stimulatory effect of insulin on potassium uptake but had only a small (and statistically insignificant) effect on forearm glucose extraction (from 20 ± 2 to 16 ± 2%, P = NS). We conclude that in human forearm muscle ouabain inhibits Na+-K+ exchange and depresses insulin-induced glucose uptake via an adrenergic-mediated limitation of blood flow. When vasoconstriction is prevented, the actions of insulin on glucose and potassium influx appear to be largely independent of one another.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
