Influence of Potassium on Blood Sugar and Tissue Glycogen

Abstract

It has been suggested that most of the disturbances observed after adrenal removal are secondary to a primary defect in potassium metabolism. 1 For the specific case in which we are interested, this is held to mean that the low blood sugar and tissue glycogen of adrenalectomized animals result from a primary rise in serum potassium. Some of the experiments we have been carrying out recently bear on this hypothesis, but lend it no credence.

Normal white rats weighing between 80 and 100 gm. were fasted for 18 hours, given intraperitoneal injections of K-free or K-containing solutions, and then serially sacrificed. When the injected solution consisted of normal sodium chloride and 5% glucose solution (10 cc. per 100 gm. rat), the blood sugar and liver and muscle glycogen curves over 3.75 hours followed the course shown in Table I. Both muscle and (especially) liver glycogen were deposited in large amounts, while the blood sugar level remained relatively stationary. But when the injected fluid contained, in addition to sodium chloride and glucose, 0.4% potassium (in the form of potassium acetate), the formation of both muscle and liver glycogen was completely suppressed, while the blood sugar level quickly rose over 100%.