For her study led by Dr. Stefan Kubicek from the CeMM in co-operation with the Université Côte d'Azur in Nice and the group of Jacob Hecksher Sorensen from Nordisk, the scientists used alpha cell cultures in a fully automated process to exclude a possible disturbing influence of other tissue types. With the cell lines, the research group was able to test their collection of active ingredients so that they finally were focised on artemisinine, an agent against malaria. Here they succeeded in elucidating the mechanism of action.

Alpha and beta cells build, together with at least three further highly specialized cell types, the so-called Langerhans islands of the pancreas, the control centers for the blood glucose level. Insulin from beta cells lowers the level, glucagon from alpha cells increases it again. However, the cells are flexible: in previous studies with model organisms it has been shown that in a case of an extreme loss of beta cells, a transformation of the alpha cells can take place balancing the damage.

It was found that the genetic main switch Arx plays a central role. In previous studies with the co-operation partners from Nice, it has been shown that a switching off of Arx via genetic methods leads to the conversion of alpha to beta cells.
 
The study is published in journal Cell.

Jin Li, Tamara Casteels, Thomas Frogne, Camilla Ingvorsen, Christian Honoré, Monica Courtney, Kilian V.M. Huber, Nicole Schmitner, Robin A. Kimmel, Roman A. Romanov, Caterina Sturtzel, Charles-Hugues Lardeau, Johanna Klughammer, Matthias Farlik, Sara Sdelci, Andhira Vieira, Fabio Avolio, Francois Briand, Igor Baburin, Peter Májek, Florian M. Pauler, Thomas Penz, Alexey Stukalov, Manuela Gridling, Katja Parapatics,
Charlotte Barbieux, Ekaterine Berishvili, Andreas Spittler, Jacques Colinge, Keiryn L. Bennett, Steffen Hering, Thierry Sulpice, Christoph Bock, Martin Distel, Tibor Harkany, Dirk Meyer, Giulio Superti-Furga, Patrick Collombat, Jacob Hecksher-Sørensen, and Stefan Kubicek (2016): Artemisinins Target GABAA Receptor Signaling and Impair α Cell Identity. Cell, December 1, 2016. DOI: 10.1016 / j.cell.2016.11.010

Source:
https://idw-online.de/en/news664359