In this double-blind, placebo-controlled study in 11 subjects (7 male, 4 female, ages 47–63 years), 90 meqs of oral KCl or Kcitrate per day for 2 weeks 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.
K+ 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.