Press releases

Type 1 diabetes : regenerate our own insulin cells ?

27 Jun 2013 | By Inserm (Newsroom) | Circulation, metabolism, nutrition

Patrick Collombat, Inserm Research Director and head of the Avenir team at the Institut de Biologie Valrose in Nice, has published new results concerning Type I diabetes. Researchers show that, in mice, the pancreas contains cells capable of being converted into insulin-producing β cells, something that can be done at any age. They also demonstrate that all pancreatic β cells can be regenerated several times and that chemically-induced diabetes in mice can thus be “treated” repeatedly. The challenge for the researchers is now to show that these procedures can be applied to humans.

This work is published online in the Developmental Cell journal dated 27 June 2013.

Type I diabetes, characterised by the selective loss of pancreatic, insulin-producing β cells, is a condition that affects more than 30 million people worldwide. Despite current treatments, type I diabetic patients have a life expectancy that is reduced by five to eight years. It is in this context that the Avenir “Diabetes Genetics” team have been working to develop new approaches designed to regenerate these cells.

In 2009, researchers at the Valrose Biology Institute (Inserm/University Nice Sophia Antipolis) managed to convert glucagon-producing α cells into β cells in young mice. Today, thanks to the use of transgenic mice, they report the mechanisms resulting in this exchange of cell identity. Specifically, they show that pancreatic ductal cells can be continuously mobilised and literally transformed into α and subsequently into β cells, a process that works at any age. Such transformation is obtained through the forced activation of the Pax4 gene in the α cells of the pancreas. The resulting cascade of events causes the generation of brand-new β cells, thanks to the reactivation of development genes. Throughout this process, α cells are regenerated and gradually adopt the profile of β cells. This means that the pancreas has a virtually inexhaustible source of cells capable of replacing the β cells.

β cell regeneration in the pancreas


© Patrick Collombat / Inserm

Left: pancreas of control mice (non-diabetic)
Right: pancreas of transgenic mice demonstrating massive regeneration of insulin-producing β cells (coloured pink) following chemical induction of diabetes.

By artificially inducing type I diabetes in mice, 

“we also show that all the pancreatic β cells can be regenerated at least three times using this mechanism. Diabetes, induced in this way, in the mouse, can be literally “treated” multiple times thanks to the new stock of functional, insulin-producing β cells”

explains Patrick Collombat, Inserm research director and principal author of the study.

These promising results obtained in the mouse suggest that the pancreas contains cells that can regenerate several times those β cells lost in type I diabetics.

“We are currently working on the possibility of inducing such regeneration by using pharmacological molecules. Thanks to this new data, we shall be concentrating in future years on determining whether these processes can also be made to work in humans, a real challenge in offering better treatments for type I diabetic patients”, he concludes.

Researcher Contact
Patrick Collombat Directeur de recherche Inserm Responsable de l'équipe AVENIR : Génétique du diabète Unité 1091 - Institut de Biologie Valrose (Inserm/Université  Nice Sophia Antipolis) rf.mresni@tabmolloc.kcirtaP 04 92 07 64 16
Press Contact
Juliette Hardy rf.mresni@esserp
Developmental Cell,  27 juin 2013 Adult duct-lining cells can reprogram into β-like cells able to counter repeated cycles of toxin-induced Diabetes Keith Al-Hasani1,2,3,4,#, Anja Pfeifer1,2,3,#, Monica Courtney1,2,,3,#, Nouha Ben-Othman1,2,3,#, Elisabet Gjernes1,2,3, Andhira Vieira1,2,3, Noémie Druelle1,2,3, Fabio Avolio1,2,3, Philippe Ravassard5, Gunter Leuckx6, Sandra Lacas-Gervais7, Damien Ambrosetti8, Emmanuel Benizri9, Jacob Hecksher-Sorensen10, Pierre Gounon7, Jorge Ferrer11, Gerard Gradwohl12, Harry Heimberg6, Ahmed Mansouri3,13,14,*, and Patrick Collombat1,2,3,15,* 1 Université de Nice-Sophia Antipolis, FR-06108 Nice, France 2 Inserm U1091, IBV, Diabetes Genetics Team, FR-06108 Nice, France 3 JDRF, 26 Broadway, NY-10004, USA 4 Present address: Epigenetics in Human Health and Disease Laboratory, Baker IDI Heart and Diabetes Institute, The Alfred Medical Research and Education Precinct, Melbourne, Victoria, 3004, Australia. 5 Biotechnology and Biotherapy Laboratory, Centre de Recherche de l’Institut du Cerveau et de la Moelle, CNRS UMR 7225; INSERM UMRS 975; University Pierre et Marie Curie, Hôpital Pitié  Salpétrière, FR-75013 Paris, France 6 Diabetes Research Center, Vrije Universiteit Brussel, Laarbeeklaan 103, B-1090 Brussel, Belgium 7 Centre Commun de Microscopie, Université de Nice-Sophia Antipolis, FR-06108 Nice, France 8 Laboratoire central d'Anatomie Pathologique, CHU de Nice, FR-06100 Nice, France 9 Chirurgie Générale et Cancérologie Digestive, CHU de Nice, FR-06100 Nice, France 10 Hagedorn Research Institute, Department of Developmental Biology, Niels Steensensvej 6, DK-2820 Gentofte, Denmark 11 Endocrinology, Hospital Clinic de Barcelona, SP-08036 Barcelona, Spain 12 Inserm U964/CNRS UMR 7104/University of Strasbourg, FR-67404 Illkirch, France 13 Max-Planck Institute for Biophysical Chemistry, Department of Molecular Cell 3iology, Am Fassberg, D-37077 Göttingen, Germany 14 Department of Clinical Neurophysiology, University of Göttingen, Robert-Koch Strasse 40, D-37075 Göttingen, Germany 15 Genome and Stem Cell Center, GENKOK, Erciyes University, 38039, Kayseri,Turkey # Authors contributed equally to this work