Conen Katrin, Scanni Roberto, Gombert Marie-Therese, Hulter Henry N, Krapf Reto
Medizinische Universitätsklinik, Kantonsspital Bruderholz, University of Basel, CH-4101 Bruderholz/Basel Switzerland.
Department of Medicine, University of California San Francisco, San Francisco, CA USA.
J Diabetes Complications. 2016 Aug;30(6):1158-61. doi: 10.1016/j.jdiacomp.2016.03.017. Epub 2016 Mar 17.
Experimental 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.
In 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.
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.
实验性钾缺乏可可逆性抑制胰岛素分泌，而慢性代谢性酸中毒会降低胰岛素敏感性。我们旨在研究在合并葡萄糖耐量异常的非酸中毒、血钾正常的人群中补充钾和碱的效果。
在这项针对11名受试者（7名男性，4名女性，年龄47 - 63岁）的双盲、安慰剂对照研究中，每天口服90毫当量氯化钾或柠檬酸钾，各持续2周，通过稳态模型评估β细胞功能发现，两者均增加了胰岛素分泌[氯化钾组 = 86（置信区间81 - 91），柠檬酸钾组 = 88（82 - 94），安慰剂组 = 78（73 - 83）%，p < 0.04]，但只有柠檬酸钾通过稳态模型评估胰岛素抵抗（HOMA - IR）减轻了胰岛素抵抗（胰岛素抵抗，柠檬酸钾组 = 2.8（2.5 - 3.1），安慰剂组 = 3.2（2.9 - 3.5），p < 0.03），且只有柠檬酸钾增加了定量胰岛素敏感性检查指数（Quicki，柠檬酸钾组 = 0.355（0.305 - 0.405），安慰剂组 = 0.320（0.265 - 0.375），p < 0.04）。这些结果通过独立测量得到证实，即在口服葡萄糖耐量试验期间测量的HOMA C肽和全身胰岛素敏感性指数。柠檬酸钾显著降低了24小时动态收缩压和舒张压（与安慰剂相比分别为 - 4.0（- 3至 - 5）和 - 2.7（- 1.9至 - 3.5），p < 0.02），而氯化钾无显著作用。
在无明显钾缺乏的情况下补充钾可改善合并葡萄糖耐量异常受试者的β细胞功能。然而，胰岛素增敏和降压作用取决于伴随的阴离子柠檬酸盐。
