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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.

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