TY - JOUR
T1 - Insulin-mediated potassium uptake is normal in uremic and healthy subjects
AU - Alvestrand, A.
AU - Wahren, J.
AU - Smith, D.
AU - DeFronzo, R. A.
PY - 1984
Y1 - 1984
N2 - We examined the ability of physiological hyperinsulinemia to enhance potassium and glucose uptake by splanchnic and peripheral tissues in 12 chronically uremic subjects by using the euglycemic insulin clamp technique in combination with hepatic and femoral venous catheterization. In control subjects, the decline in plasma potassium concentration averaged 0.95 ± 0.05 meq/liter. Splanchnic (67 ± 10.3 μeq/min) and leg (22.2 ± 1.4 μeq/min) potassium uptake accounted for 43 and 59% respectively, of the total amount of potassium that was translocated from the extracellular to intracellular fluid compartment. In uremic individuals, the decline in plasma potassium concentration (0.98 ± 0.10) was similar to controls. Likewise, the mean splanchnic (66.6 ± 6.1 μeq/min) and leg (22.4 ± 1.6 μeq/min) potassium uptakes were similar to controls. These results indicate that insulin-mediated potassium uptake is not altered by uremia. In contrast, insulin-mediated potassium glucose uptake is markedly impaired. These observations suggest that the various actions of insulin can be differentially impaired by uremia and the steps distal to the insulin receptor must be responsible for the insulin resistance.
AB - We examined the ability of physiological hyperinsulinemia to enhance potassium and glucose uptake by splanchnic and peripheral tissues in 12 chronically uremic subjects by using the euglycemic insulin clamp technique in combination with hepatic and femoral venous catheterization. In control subjects, the decline in plasma potassium concentration averaged 0.95 ± 0.05 meq/liter. Splanchnic (67 ± 10.3 μeq/min) and leg (22.2 ± 1.4 μeq/min) potassium uptake accounted for 43 and 59% respectively, of the total amount of potassium that was translocated from the extracellular to intracellular fluid compartment. In uremic individuals, the decline in plasma potassium concentration (0.98 ± 0.10) was similar to controls. Likewise, the mean splanchnic (66.6 ± 6.1 μeq/min) and leg (22.4 ± 1.6 μeq/min) potassium uptakes were similar to controls. These results indicate that insulin-mediated potassium uptake is not altered by uremia. In contrast, insulin-mediated potassium glucose uptake is markedly impaired. These observations suggest that the various actions of insulin can be differentially impaired by uremia and the steps distal to the insulin receptor must be responsible for the insulin resistance.
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U2 - 10.1152/ajpendo.1984.246.2.e174
DO - 10.1152/ajpendo.1984.246.2.e174
M3 - Article
C2 - 6364842
AN - SCOPUS:0021378264
SN - 0193-1849
VL - 9
SP - E174-E180
JO - American Journal of Physiology - Endocrinology and Metabolism
JF - American Journal of Physiology - Endocrinology and Metabolism
IS - 2
ER -