The mechanism by which potassium deficiency per se impairs glucose tolerance was studied in seven subjects who were potassium depleted experimentally (mean depletion = 326 mEq.).
In five subjects studied using the oral glucose tolerance test, all showed impairment during the potassium depletion phase compared to the predepletion control period, and four of five subjects showed improvement with potassium repletion. The four subjects with impaired glucose tolerance compared to both control periods showed a delay in the initial phase of total immunoreactive insulin release. None of the five subjects showed a significant variation in the per cent proinsulin-like component from the potassium depletion phase to either control period. Two subjects studied using the intravenous glucose tolerance test showed no impairment of glucose tolerance with potassium depletion, and no evidence of insulin resistance was found following the injection of 0.05 U. per kilogram of insulin. These two subjects did manifest impaired growth hormone responses to the hypoglycemic stimulus, however.
Potassium depletion per se impairs glucose tolerance. The defect is mild; severe glucose intolerance, alterations in total immunoreactive insulin, and plasma insulin components seen in clinical hypokalemic states involve a complex interplay between potassium deficiency and the primary disease state.