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

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82 Citations (Scopus)


The incretin hormone glucagon-like peptide 1 (GLP-1) promotes glucose homeostasis and enhances b-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 (3040%) on GLP-1stimulated insulin secretion during hyperglycemic clamps in nondiabetic Caucasian individuals (TMEM114; CHST3 and CTRB1/2; n = 232; all P ≤8.8 × 10
Original languageEnglish
Pages (from-to)3275-3281
Issue number9
Early online date14 May 2013
Publication statusPublished - 2013

Cohort Studies

  • Netherlands Twin Register (NTR)

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