AIMS: The voltage-gated potassium channel K v 11.1 is important for repolarising the membrane potential in excitable cells such as myocytes, pancreatic α- and β-cells. Moxifloxacin blocks the K v 11.1 channel and increases the risk of hypoglycaemia in patients with diabetes. We investigated glucose regulation and secretion of glucoregulatory hormones in young people with and without moxifloxacin a drug known to block the K v 11.1 channel.

MATERIAL AND METHODS: The effect of moxifloxacin (800 mg/day for four days) or placebo on glucose regulation was assessed in a randomised, double-blind, crossover study of young men and women (age 20-40 years and BMI 18.5-27.5 kg/m 2 ) without chronic disease, using 6-hour oral glucose tolerance tests (OGTT) and continuous glucose monitoring (CGM).

RESULTS: Thirty-eight participants completed the study. Moxifloxacin prolonged the QTcF-interval and increased heart rate. Hypoglycaemia was more frequently observed with moxifloxacin, both during the eight days of CGM and during the OGTT. Hypoglycaemia questionnaire scores were higher after intake of moxifloxacin. Moxifloxacin reduced early plasma-glucose response (AUC 0-30min ) by 7% (95%CI: -9% to -4%, p<0.01), and overall insulin response (AUC 0-360min ) decreased by 18% (95%CI: -24% to -11%, p<0.01) and plasma glucagon increased by 17% (95%CI: 4% to 33%, p=0.03). Insulin sensitivity calculated as Matsuda index increased by 11%, and MISI, an index of muscle insulin sensitivity, increased by 34%.

CONCLUSIONS: In young men and women, moxifloxacin a drug known to block the K v 11.1 channel increased QT interval, decreased glucose levels, and was associated with increased muscle insulin sensitivity and more frequent episodes of hypoglycaemia. This article is protected by copyright. All rights reserved.