Disturbances in glucose and insulin metabolism frequently accompany a variety of clinical states associated with potassium deficiency. The exact role of the potassium deficit and the mechanism of its effect are in doubt. The glucose-clamp technique was therefore employed to study glucose and insulin metabolism in 7 normal young male subjects before and after induction of potassium depletion. The clamp technique places the blood glucose concentration under the investigator's control. Under the conditions of steady state hyperglycemia (125 mg/dl above basal for 2 hr) it provides quantification of (1) pancreatic beta cell sensitivity to glucose (plasma insulin response), (2) glucose tolerance (glucose metabolized), and (3) tissue sensitivity to insulin (glucose metabolized/insulin response). Potassium deficiency was induced during a 7-8 day period of a weight-maintaining diet containing 40 meq potassium and at least 150 g carbohydrate, along with the administration of 60 g Na polystyrene sulfonate daily. Paired analysis showed a significant decline in the amount of glucose metabolized from pre- to postdepletion (-27.4 ± 4.5%, p < 0.01). This decline in carbohydrate tolerance was associated with a significant decrease in plasma insulin response to sustained hyperglycemia (-26% ± 6.9%, p < 0.02). Potassium depletion had no effect on tissue sensitivity to insulin (+1.7 ± 7.8%). The degree of potassium depletion as estimated by change in total body 40K ranged from 1.0% to 8.4% and correlated with the decrease in insulin response (r = 0.78, p < 0.05). This study demonstrates that potassium depletion causes glucose intolerance, which is associated with impaired insulin secretion.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism