Effect of graded doses of insulin on splanchnic and peripheral potassium metabolism in man

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Abstract
The effect of insulin on K metabolism was examined in 29 healthy volunteers employing the insulin clamp technique with graded doses of insulin in combination with the hepatic venous catheter technique. The plasma insulin concentration was acutely raised and maintained at 27 .+-. 4, 51 .+-. 6, 100 .+-. 7, 428 .+-. 37, or 1191 .+-. 12 .mu.U[units]/ml, while the plasma glucose concentration was held constant at the basal level by a variable glucose infusion. A dose-related decline in plasma K concentration was observed that varied between 0.58 .+-. 0.12 and 1.54 .+-. 0.23 meq/l. During the 1st h of the insulin infusion, a marked increase in splanchnic K uptake occurred and accounted for approximately 70% of the decline in extracellular fluid K content. Splanchnic K uptake showed a positive correlation (r [correlation coefficient] = 0.864, P < 0.001) with the decrease in plasma K concentration. During the 2nd h after insulin, splanchnic K balance returned to or below basal levels and an inverse correlation (r = -0.555, P < 0.05) between the fall in plasma K and net splanchnic balance was observed. In virtually all patients in whom the plasma K fell more than 1 meq/l below basal, a net splanchnic efflux of K was observed during the 2nd h. When a simultaneous infusion of KCl was given with insulin to prevent hypokalemia, splanchnic K balance remained markedly positive throughout the 2 h study. The decline in plasma K concentration was closely correlated with both the plasma insulin concentration and the total amount of glucose metabolized. In contrast, net splanchnic K balance showed no significant relationship to net glucose uptake by the splanchnic bed. Insulin causes a dose-related decline in the plasma K concentration that is progressive with time. During the 1st h after insulin administration, the majority of the decline in plasma K concentration can be accounted for by net splanchnic K uptake. However, during the 2nd h after insulin, splanchnic K balance returns to or below basal levels, and peripheral tissues are primarily responsible for the continued fall in plasma K concentration. Hypokalemia contributes, at least in part, to the reversal in net splanchnic K balance observed after 1 h of insulin infusion. Insulin-mediated splanchnic K uptake is not dependent on net splanchnic glucose uptake.