{"id":"doi:10.1007/s00125-017-4289-0","kind":"article","title":"Effects of semaglutide on beta cell function and glycaemic control in participants with type 2 diabetes: a randomised, double-blind, placebo-controlled trial","authors":["Kapitza C","Dahl K","Jacobsen JB","Axelsen MB","Flint A"],"author_count":5,"year":2017,"published":"2017-05-19","venue":"Diabetologia","cited_by":97,"doi":"10.1007/s00125-017-4289-0","arxiv_id":null,"nct_id":null,"source_url":"https://doi.org/10.1007/s00125-017-4289-0","archive_url":"https://space-kitty.com/papers/doi:10.1007/s00125-017-4289-0","updated":null,"pmid":"28526920","pmcid":"PMC5491562","openalex_id":null,"pdf_url":"https://europepmc.org/articles/PMC5491562/pdf","abstract":"Aims/hypothesis Semaglutide is a glucagon-like peptide-1 analogue in development for the treatment of type 2 diabetes. Its effects on first- and second-phase insulin secretion and other measures of beta cell function and glycaemic control were assessed. Methods In this single-centre, double-blind, placebo-controlled, parallel-group trial, conducted at the Profil Institut für Stoffwechselforschung, Germany, 75 adult (aged 18-64 years) participants with type 2 diabetes (eligibility: HbA 1c of 6.5-9.0% (47.5-74.9 mmol/mol); BMI 20.0-35.0 kg/m 2 ; and treatment with diet and exercise and/or metformin monotherapy with a dose unchanged in the 30 days prior to screening) were randomised (1:1) to once-weekly s.c. semaglutide 1.0 mg (0.25, 0.5, 1.0 mg escalated) or placebo for 12 weeks. Co-primary endpoints were changes from baseline to end of treatment in the first (AUC 0-10 min ) and second (AUC 10-120 min ) insulin secretion phases, as measured by the IVGTT. An arginine stimulation test (AST) and a 24 h meal stimulation test were also conducted. A graded glucose infusion test (GGIT) assessed insulin secretion rate (ISR) in treated participants and a group of untreated healthy participants. Safety endpoints were also assessed. Results In total, 37 participants received semaglutide and 38 received placebo. Following IVGTT, for insulin, both AUC 0-10min and AUC 10-120min were significantly increased with semaglutide (estimated treatment ratio [95% CI] 3.02 [2.53, 3.60] and 2.10 [1.86, 2.37], respectively; p < 0.0001). The 24 h meal test showed reduced fasting, postprandial and overall (AUC 0-24h ) glucose and glucagon responses with semaglutide (p < 0.0001). The AST showed that maximal insulin capacity increased following semaglutide treatment. During GGIT, semaglutide significantly increased ISR to levels similar to those in healthy participants. Semaglutide was well tolerated. Conclusions/interpretation Twelve weeks of once-weekly treatment with semaglutide significantly improved beta cell function and glycaemic control in participants with type 2 diabetes. Trial registration ClinicalTrials.gov NCT02212067 FUNDING: The study was funded by Novo Nordisk A/S.","abstract_license":"CC-BY (article license as recorded by Europe PMC; abstract reproduced unmodified apart from markup removal)","license":"CC-BY","is_open_access":true,"retracted":false,"peer_reviewed":null,"categories":[],"details":null,"provenance":"europepmc","attribution":"Abstract of \"Effects of semaglutide on beta cell function and glycaemic control in participants with type 2 diabetes: a randomised, double-blind, placebo-controlled trial\" by Kapitza C, Dahl K, Jacobsen JB et al., https://doi.org/10.1007/s00125-017-4289-0, used under its Creative Commons Attribution license (CC-BY); markup removed, otherwise unmodified.","topics":[{"slug":"glp1-metabolic","name":"GLP-1 & Incretin Therapies","domain_slug":"medicine"}],"cited_in_dossiers":[]}