The work of Y.L. was supported by grant KO 3598/4-2 . The work of P. Schlosser was supported by the German Research Foundation project ID 1050086601 and the EQUIP Program for Medical Scientists, Faculty of Medicine, University of Freiburg. The work of S.H., M.W., P. Sekula, M.K., M.S. and A.K. was supported by the DFG project ID 431984000 . The work of F. Kotsis and U.T.S.
Institute of Genetic Epidemiology, Faculty of Medicine and Medical Center - University of Freiburg, Freiburg, Germany Pascal Schlosser, Nora Scherer, Franziska Grundner-Culemann, Sara Monteiro-Martins, Stefan Haug, Inga Steinbrenner, Burulça Uluvar, Matthias Wuttke, Yurong Cheng, Fruzsina Kotsis, Ulla T. Schultheiss, Peggy Sekula, Yong Li & Anna KöttgenPascal Schlosser, Josef Coresh & Anna KöttgenNora Scherer
Institute of Human Genetics, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen–Nürnberg, Erlangen, GermanyMembrane Transport Discovery Lab, Department of Nephrology and Hypertension and Department of Biomedical Research, University of Bern, Bern, SwitzerlandEdward D. Karoly & Robert P. Mohney
Department of Medicine IV—Nephrology and Primary Care, Faculty of Medicine and Medical Center, University of Freiburg, Freiburg, GermanyResearch and Early Development, Pharmaceuticals Division, Bayer AG, Wuppertal, GermanyDepartment of Clinical Sciences in Malmö, Lund University Diabetes Centre, Lund University, Lund, SwedenEpidemiology, Human Genetics and Environmental Sciences, School of Public Health, University of Texas Health Science Center at Houston, Houston, TX, USAMorgan E.
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Genome-wide association analysis identifies ancestry-specific genetic variation associated with acute response to metformin and glipizide in SUGAR-MGH - DiabetologiaAims/hypothesis Characterisation of genetic variation that influences the response to glucose-lowering medications is instrumental to precision medicine for treatment of type 2 diabetes. The Study to Understand the Genetics of the Acute Response to Metformin and Glipizide in Humans (SUGAR-MGH) examined the acute response to metformin and glipizide in order to identify new pharmacogenetic associations for the response to common glucose-lowering medications in individuals at risk of type 2 diabetes. Methods One thousand participants at risk for type 2 diabetes from diverse ancestries underwent sequential glipizide and metformin challenges. A genome-wide association study was performed using the Illumina Multi-Ethnic Genotyping Array. Imputation was performed with the TOPMed reference panel. Multiple linear regression using an additive model tested for association between genetic variants and primary endpoints of drug response. In a more focused analysis, we evaluated the influence of 804 unique type 2 diabetes- and glycaemic trait-associated variants on SUGAR-MGH outcomes and performed colocalisation analyses to identify shared genetic signals. Results Five genome-wide significant variants were associated with metformin or glipizide response. The strongest association was between an African ancestry-specific variant (minor allele frequency [MAFAfr]=0.0283) at rs149403252 and lower fasting glucose at Visit 2 following metformin (p=1.9×10−9); carriers were found to have a 0.94 mmol/l larger decrease in fasting glucose. rs111770298, another African ancestry-specific variant (MAFAfr=0.0536), was associated with a reduced response to metformin (p=2.4×10−8), where carriers had a 0.29 mmol/l increase in fasting glucose compared with non-carriers, who experienced a 0.15 mmol/l decrease. This finding was validated in the Diabetes Prevention Program, where rs111770298 was associated with a worse glycaemic response to metformin: heterozygous carriers had an increase in HbA1c of
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