The CTRB1/2 locus affects diabetes susceptibility and treatment via the incretin pathway

L.M. t Hart, A. Fritsche, G. Nijpels, N. van Leeuwen, L.A. Donnelly, J.M. Dekker, M. Alssema, J. Fadista, F. Carlotti, A.P. Gjesing, C.N. Palmer, T.W. van Haeften, S.A. Herzberg-Schafer, A.M. Simonis-Bik, J.J. Houwing-Duistermaat, Q. Helmer, J. Deelen, B. Guigas, T. Hansen, F. MachicaoG. Willemsen, R.J. Heine, M.H. Kramer, J.J. Holst, E.J. de Koning, H.U. Haring, O. Pedersen, L. Groop, E.J. de Geus, P.E. Slagboom, D.I. Boomsma, E.M. Eekhoff, E.R. Pearson, M. Diamant

Research output: Contribution to journal/periodicalArticleScientificpeer-review

Abstract

The incretin hormone glucagon-like peptide 1 (GLP-1) promotes glucose homeostasis and enhances beta-cell function. GLP-1 receptor agonists (GLP-1 RAs) and dipeptidyl peptidase-4 (DPP-4) inhibitors, which inhibit the physiological inactivation of endogenous GLP-1, are used for the treatment of type 2 diabetes. Using the Metabochip, we identified three novel genetic loci with large effects (30-40%) on GLP-1-stimulated insulin secretion during hyperglycemic clamps in nondiabetic Caucasian individuals (TMEM114; CHST3 and CTRB1/2; n = 232; all P
Original languageEnglish
Pages (from-to)3275-3281
JournalDiabetes
Volume62
Issue number9
DOIs
Publication statusPublished - 2013

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