Effects of potassium citrate or potassium chloride in patients with combined glucose intolerance: A placebo-controlled pilot study

Abstract

BackgroundExperimental K+ depletion reversibly inhibits insulin secretion, while chronic metabolic acidosis decreases insulin sensitivity. We aimed to investigate the effects of potassium supplementation and alkali supplementation in non-acidotic, normokalemic humans with combined glucose intolerance. Study design and resultsIn this double-blind, placebo-controlled study in 11 subjects (7 male, 4 female, ages 47–63 years), 90meqs of oral KCl or Kcitrate per day for 2weeks each increased insulin production as measured by homeostasis model assessment Beta [KCl=86 (CI 81–91), Kcitrate=88 (82–94), placebo=78 (73–83)%, p<0.04], but only Kcitrate attenuated insulin resistance as assessed by HOMA-IR (insulin resistance, Kcitrate=2.8 (2.5–3.1), placebo=3.2 (2.9–3.5), p<0.03) and only Kcitrate increased quantitative insulin sensitivity check index (Quicki, Kcitrate=0.355 (0.305–0.405), placebo=0.320 (0.265–0.375) p<0.04). These results were confirmed by independent measurements, i.e. HOMA C-peptide and whole body insulin sensitivity index measured during oral glucose tolerance testing. Kcitrate significantly decreased systolic and diastolic 24-hour ambulatory blood pressures (−4.0 (−3 to −5) and −2.7 (−1.9 to −3.5), respectively as compared to placebo, p<0.02) while KCl was without a significant effect. ConclusionsK+ supplementation in the absence of overt K+ depletion improves beta-cell function in subjects with combined glucose intolerance. The insulin-sensitizing and hypotensive effect, however, depend on citrate as the accompanying anion.