Aim: The voltage-gated potassium channel K v 11.1 is important for repolarizing the membrane potential in excitable cells such as myocytes, pancreatic αand 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. Materials and Methods:The effect of moxifloxacin (800 mg/day for 4 days) or placebo on glucose regulation was assessed in a randomized, double-blind, crossover study of young men and women (age 20-40 years and body mass index 18.5-27.5 kg/m 2 ) without chronic disease, using 6-h oral glucose tolerance tests and continuous glucose monitoring.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 8 days of continuous glucose monitoring and during the oral glucose tolerance tests. Hypoglycaemia questionnaire scores were higher after intake of moxifloxacin. Moxifloxacin reduced the early plasmaglucose response (AUC 0-30 min ) by 7% (95% CI: À9% to À4%, p < .01), and overall insulin response (AUC 0-360 min ) decreased by 18% (95% CI: À24% to À11%, p < .01) and plasma glucagon increased by 17% (95% CI: 4%-33%, p = .03). Insulin sensitivity calculated as the 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

Objective: The aim of this study was to investigate glucose tolerance, glucagon response, and beta cell function during a 1-year maintenance period with either exercise, the glucagon-like peptide-1 receptor agonist liraglutide, or the combination after diet-induced weight loss.Methods: In this randomized placebo-controlled trial, adults with obesity (BMI: 32-43 kg/m 2 ) without diabetes underwent an 8-week low-calorie diet (800 kcal/d) and were randomized to 52 weeks of aerobic exercise, liraglutide 3.0 mg/d, exercise and liraglutide combined, or placebo. Change in glucose and glucagon response to a 3-hour mixed meal test and disposition index, as a measure of beta cell function, were measured.Results: A total of 195 participants were randomized. After 1 year of treatment, the combination group had decreased postprandial glucose response by À9% (95% CI: À14% to À3%; p = 0.002), improved beta cell function by 49% (95% CI: 16% to 93%; p = 0.002), and decreased glucagon response by À18% (95% CI: À34% to À3%; p = 0.024) compared with placebo. Compared with placebo, liraglutide alone improved postprandial glucose response by À7% (95% CI: À12% to À1%; p = 0.018), but not beta cell function or glucagon. Exercise alone had similar postprandial glucose response, beta cell function, and glucagon response as placebo.Conclusions: Only the combination of exercise and liraglutide improved glucose tolerance, beta cell function, and glucagon responses after weight loss.