Störungen des Kohlenhydratstoffwechsels im Kaliummangel

Summary

Feeding rats a low potassium diet over a period of 2–3 weeks produces a negative potassium balance the mean of which is 1445±125 μeq/animal.

Blood glucose concentration has been found increased under this condition. Following intravenous loading with glucose there is a decrease in the elimination constant k ₂ of glucose. Cellular glucose uptake has also been found to be impaired in alloxan diabetic animals fed a low potassium diet. From this it is concluded that there is a reduction in basal glucose transport in potassium deficiency. L-arabinose distribution volume is also decreased, indicating that the impairment in cellular glucose uptake is not caused by a reduction in intracellular utilisation of glucose. Endogenous insulin has been found to accelerate impaired basal glucose transport to a smaller degree than the unimpaired glucose transport in normal rats. Insulin plasma concentration is elevated. The same applies to the pancreatic function to secrete insulin in response to an increase in blood glucose concentration. The increase in insulin secretion is considered to be the consequence of the diminished action of insulin. The same relation holds for experiments in which glucocorticoids were given to rats at a pharmacological dose level: as glucocorticoids diminish basal glucose uptake, insulin secretion increases, apparently to compensate for the impaired peripheral action of endogenous insulin.

The reduction in basal glucose transport as well as its consequences on insulin secretion in potassium deficient rats may partly be caused by an increase in glucocorticoid secretion. This has been concluded from an increase in suprarenal corticosterone concentration. An enhanced rate of corticosterone synthesis and output may be responsible for the increase in hepatic and renal glucose-6-phosphatase activity of potassium depleted rats.

Lowering intracellular pH values has also been found to lead to an increase in hepatic glucose-6-phosphatase activity. Therefore, an intracellular acidosis in liver could contribute to the increase in glucose-6-phosphatase activity measured in the liver of potassium deficient rats. Cellular acidosis has been found to occur in skeletal muscles of potassium deficient animals, and this was explained by hydrogen ions partially replacing the decrease in intracellular potassium concentration (Cooke, Segar, Cheek, Coville, and Darrow, 1952; Irvine, Saunders, Milne, and Crawford, 1960). Cellular sodium and potassium concentration are, however, unaltered in the liver of potassium deficient rats. Thus, there is no indication for a compensatory increase in intracellular hydrogen concentration in this tissue.

In contrast to liver, besides the glucocorticoid induced effect a pH dependent increase in glucose-6-phosphatase activity may contribute to the increase in enzymic hydrolysis of glucose-6-phosphate observed in the kidneys of potassium depleted rats.

In addition to the replacement of cellular potassium by hydrogen ions there is also a compensatory increase in intracellular sodium concentration of skeletal muscles. Sodium ions inhibit glycogen phosphorylase phosphatase thereby reducing the rate of conversion of active glycogen phosphorylase a into the inactive glycogen phosphorylase b. Consequently, the glycogenolytic action of epinephrine is increased in potassium deficiency.