Daisuke Yabe1, Anu Ambos2, Bertrand Cariou3, Lea Duvnjak4, Marc Evans5, Guillermo González-Gálvez6, Jay Lin7, Elena V Nikonova8, Pedro de Pablos-Velasco9, Jean-François Yale10, Bo Ahrén11. 1. Kansai Electric Power Hospital, 2-1-7 Fukushima, Fukushima-ku, Osaka 553-0003, Japan; Kansai Electric Power Medical Research Institute, 1-5-6 Minatojimaminamimachi, Chuo-ku, Kobe 650-0047, Japan; Kobe University Graduate School of Medicine, 1-5-6 Minatojimaminamimachi, Chuo-ku, Kobe 650-0047, Japan. Electronic address: ydaisuke-kyoto@umin.ac.jp. 2. North Estonia Medical Center, 19 Sütiste Street, 13419 Tallinn, Estonia. Electronic address: Anu.Ambos@regionaalhaigla.ee. 3. The Thorax Institute, CHU Nantes, Boulevard Jacques Monod, F-44093 Nantes, France. Electronic address: Bertrand.Cariou@univ-nantes.fr. 4. Vuk Vrhovac Clinic-Merkur University Hospital, University of Zagreb, Dugi dol 4a, 10000 Zagreb, Croatia. Electronic address: lduvnjak@idb.hr. 5. University Hospital Llandough, Penlan Road Llandough, CF64 2XX, UK. Electronic address: marcevans4@sky.com. 6. Jalisco Institute of Diabetes and Obesity Research SC, Morelos 1952, Guadalajara, CP 44600, Mexico. Electronic address: doctorggg@gmail.com. 7. Novosys Health, 7 Crestmont Court, Flemington, NJ 08822, USA. Electronic address: jay.lin@novosyshealth.com. 8. Artech Information Systems, LLC, 360 Mt. Kemble Ave. #2000, Morristown, NJ 07960, USA. Electronic address: Elena.Nikonova@sanofi.com. 9. Research Institute of Biomedical and Health Sciences (IUIBS), University of Las Palmas de Gran Canaria, Barranco de la Ballena sn, 35010 Las Palmas de Gran Canaria, Spain. Electronic address: pablos.velasco@ulpgc.es. 10. McGill University, 687 Pine Avenue West, Montréal, QC H3A 1A1, Canada. Electronic address: jean-francois.yale@mcgill.ca. 11. Lund University, Sölvegatan 19, SE-22184 Lund, Sweden. Electronic address: bo.ahren@med.lu.se.
Abstract
AIMS: To evaluate the impact of β-cell function on the efficacy of lixisenatide, a once-daily prandial glucagon-like peptide-1 receptor agonist, in patients with type 2 diabetes (T2D). MATERIALS AND METHODS: In this post hoc analysis, patients from the Phase 3 GetGoal-M and GetGoal-S clinical trials randomized to lixisenatide 20μg once daily were stratified into quartiles by baseline β-cell function, as measured by the secretory units of islet in transplantation (SUIT) index. RESULTS: Patients (N=437) were distributed evenly among SUIT index quartiles 1 to 4 (lowest to highest β-cell function). Clinical outcomes improved from baseline across all SUIT quartiles; mean changes at week 24 were: glycated hemoglobin (HbA1c; % [mmol/mol]), -0.99 (-10.8), -0.87 (-9.5), -0.86 (-9.4), -0.83 (-9.1); and postprandial plasma glucose (PPG; mmol/L), -7.9, -5.6, -5.5, -4.3 (overall effect P<0.0001). Furthermore, postprandial glucagon was reduced in all SUIT quartiles, while insulinogenic index improved only in patients with higher baseline SUIT (overall effect P=0.0286). No severe symptomatic hypoglycemic events were reported. CONCLUSIONS:Lixisenatide treatment resulted in reductions in HbA1c and PPG levels across all SUIT quartiles. This suggests that non-insulin-related actions of lixisenatide contribute to improved glycemic control in T2D.
RCT Entities:
AIMS: To evaluate the impact of β-cell function on the efficacy of lixisenatide, a once-daily prandial glucagon-like peptide-1 receptor agonist, in patients with type 2 diabetes (T2D). MATERIALS AND METHODS: In this post hoc analysis, patients from the Phase 3 GetGoal-M and GetGoal-S clinical trials randomized to lixisenatide 20μg once daily were stratified into quartiles by baseline β-cell function, as measured by the secretory units of islet in transplantation (SUIT) index. RESULTS:Patients (N=437) were distributed evenly among SUIT index quartiles 1 to 4 (lowest to highest β-cell function). Clinical outcomes improved from baseline across all SUIT quartiles; mean changes at week 24 were: glycated hemoglobin (HbA1c; % [mmol/mol]), -0.99 (-10.8), -0.87 (-9.5), -0.86 (-9.4), -0.83 (-9.1); and postprandial plasma glucose (PPG; mmol/L), -7.9, -5.6, -5.5, -4.3 (overall effect P<0.0001). Furthermore, postprandial glucagon was reduced in all SUIT quartiles, while insulinogenic index improved only in patients with higher baseline SUIT (overall effect P=0.0286). No severe symptomatic hypoglycemic events were reported. CONCLUSIONS:Lixisenatide treatment resulted in reductions in HbA1c and PPG levels across all SUIT quartiles. This suggests that non-insulin-related actions of lixisenatide contribute to improved glycemic control in T2D.
Authors: Ádám G Tabák; John Anderson; Pablo Aschner; Minzhi Liu; Aramesh Saremi; Peter Stella; Francisco J Tinahones; Carol Wysham; Juris J Meier Journal: Diabetes Ther Date: 2019-12-17 Impact factor: 2.945
Authors: Stefano Del Prato; Juan Pablo Frias; Lawrence Blonde; Vanita R Aroda; Niam Shehadeh; Aramesh Saremi; Terry Dex; Elisabeth Niemoeller; Elisabeth Souhami; Minzhi Liu; Julio Rosenstock Journal: Diabetes Obes Metab Date: 2020-05-28 Impact factor: 6.577
Authors: Chantal Mathieu; Stefano Del Prato; Fady T Botros; Vivian T Thieu; Imre Pavo; Nan Jia; Axel Haupt; Chrisanthi A Karanikas; Luis-Emilio García-Pérez Journal: Diabetes Obes Metab Date: 2018-05-02 Impact factor: 6.577