Der Einflu� von Insulin auf den Kaliumtransport in der Skeletmuskulatur

Abstract

The ability of insulin to increase the l-arabinose distribution volume in alloxan diabetic rats has been found decreased in 6-aminonicotinamide (6-AN) treated rats. The percentage decrease is equal to the impairment in the insulin dependent glucose transport. From this it has been concluded that the 6-AN induced impairment of the glucose diffusion facilitated by insulin is localized in the cellular membrane. Insulin plasma concentration has been found increased in 6-AN treated animals in response to an accelerated glycogenolysis mediated by an increase in epinephrine secretion. The increase in insulin secretion has been shown to cause an activation in potassium transport in skeletal muscle. Alloxan diabetic animals do not exhibit the stimulation in net cellular potassium uptake nor do adrenalectomized rats the plasma insulin concentration of which does not rise because of the lack in epinephrine mediated glycogenolysis. With especially high rates of epinephrine induced glycogenolysis plasma insulin concentration has been found to increase to a smaller degree than would be expected from the blood glucose concentration of these animals. In accordance to the results published byCoore andRandle (1964) andPorte, Graber, Kuzuya, andWilliams (1966) it is assumed that higher concentrations of epinephrine are capable to suppress insulin secretion in spite of an increase in blood glucose concentration.