Effects of potassium supplementation on insulin binding and insulin action in human obesity: protein‐modified fast and refeeding

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Abstract
To investigate the role of K deficiency in the development of glucose intolerance during caloric deprivation, K balance was maintained within normality by oral K supplementation in a group of obese subjects who underwent protein-modified fast; the results of the study of carbohydrate metabolism (oral glucose test, insulin receptors on monocytes and peripheral glucose utilization as assessed by euglycemia clamp) were compared with those obtained in a group of obese subjects admitted to protein-modified fast without K supplementation. Caloric deprivation without oral K supplementation was followed by a negative K balance and a decrease of serum K levels; a decrease of the peripheral levels of insulin, along with an increase in insulin receptors and a striking reduction of peripheral glucose utilization, were also observed. The maintenance of normal K balance and normal serum K levels with oral K-Cl supplementation was associated with higher peripheral levels of insulin (P < 0.01) and improvement of peripheral glucose utilization (P < 0.01); the binding of insulin to monocytes was unchanged. K depeletion during protein-modified fast causes a decrease of the peripheral levels of insulin and a resistance to insulin action at the postreceptors sites, which is reversed by K supply.

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