Vincent Poitout

Accredited Professor

Contact Information

Département de médecine
Centre de Recherche du Diabète de Montréal
CRCHUM, Tour Viger, 900
, rue St-Denis
Montréal (Québec)
H2X 0A9


T 514 890-8000, poste 23603 (bureau)
Site web


Our group is involved with 4 research projects:

  1. Mechanisms by which fatty acids acutely stimulate insulin secretion, and more precisely the role of the GPR40 receptor. Using GPR40 knock-out mice, we have shown that GPR40 mediates approximately 50% of the stimulatory effect of fatty acids on insulin secretion in vitro and in vivo, but is not implicated in their long-term, deleterious effects on beta-cell function.  We are currently generating a mouse line with beta-cell specific deletion of GPR40.
  2. We are studying the molecular mechanisms by which chronic fatty acids inhibit insulin gene expression. We have shown that this involves a blockade of the nuclear translocation of the transcription factor Pdx-1, as well as reduced expression of the transcription factor MafA. We are currently investigating the signaling pathways involved in palmitate inhibition of insulin gene expression.
  3. We have established an in vivo model of nutrient excess by chronic perfusion in the rat. In collaboration with the group of Marc Prentki, we are now examining the effects of age and genetic predisposition on the development of diabetes in this model.  Nous avons mis au point un modèle d’excès en nutriments chez le rat par perfusion chronique, et évaluons, en collaboration avec le groupe de Marc Prentki, les effets de l’âge et de la prédisposition génétique sur le développement du diabète.
  4. In collaboration with the group of Richard Smith at the Pacific Northwest National Laboratories in Richmond, WA, we are carrying out a study which aims to perform proteomics and metabolomics profiling of isolated human islets and to determine if changes in these global profiles correlate with islet function in vitro and in vivo, to establish predictive criteria of islet function prior to transplantation.


  • D.K. Hagman, M.G. Latour, S.K. Chakrabarti, G. Fontes, J. Amyot, C. Tremblay, M. Semache, J.A. Lausier, V. Roskens, R.G. Mirmira, T.L. Jetton, V. Poitout.  Cyclical and alternating infusions of glucose and intralipid in rats inhibit insulin gene expression and Pdx-1 binding in Islets.  Diabetes 2008, 57:424-431.
  • M. Kebede, T. Alquier, M.G. Latour, M. Semache C. Tremblay, V. Poitout. The Fatty-Acid Receptor GPR40 Plays a Role in Insulin Secretion In Vivo After High-Fat Feeding. Diabetes 2008, 57:2432-2437.
  • G. Fontés, M. Semache, D. Hagman, C. Tremblay, R. Shah, C.J. Rhodes, J. Rutter, V. Poitout. Involvement of PAS Kinase and ERK ½ in palmitate inhibition of insulin gene expression in pancreatic beta cells. Diabetes 58: 2048-2058,2009.
  • T. Alquier, M-L. Peyot, M. G. Latour, M. Kebede, C.M. Sorensen, S. Gesta, C.R. Kahn, R.D. Smith, T.L. Jetton, T.O. Metz, M. Prentki, V. Poitout. Deletion of GPR40 Impairs glucose-induced insulin secretion in vivo in mice without affecting intracellular fuel metabolism in islets. Diabetes, 2009 Nov; 58(11): 2607-15.
  • G. Fontes, G. K. Hagman, M. G. Latour, M. Semache, V. Poitout. Lack of preservation of insulin gene expression by a glucagon-like peptide 1 agonist or a dipeptidyl peptidase 4 inhibitor in an in vivo model of glucolipotoxicity. Diabetes Research and Clinical Practive, 2010 Mar; 87(3):322-8.