Scientific topics
Keywords
ITMO
Magalie Ravier PhD Endocrinology Diabetes
Course and current status
From 2021: Researcher, CRCN INSERM, Institut de Genomique Fonctionnelle, team Innovative therapeutics for diabetes, Montpellier, France.
From 2019: Associate Editor Frontiers in Endocrinology: Diabetes molecular mechanisms. https://loop.frontiersin.org/people/754128/editorial.
2015-2021 : Co-leader of the team physiopathology of pancreatic beta cells, Montpellier, France.
2009-2015: Researcher, CR1 INSERM, Institut de Genomique Fonctionnelle, team physiopathology of pancreatic beta cells, Montpellier, France.
2006-2009: Postdoc in Jean-Claude Henquin's lab, University of Louvain, Unit of Endocrinology and Metabolism, Brussels, Belgium.
2002-2006: Postdoc in Guy A Rutter's lab (now in Imperial College London), University of Bristol, Department of Biochemistry in the laboratory , Bristol, UK.
1997-2002: PhD student in Jean-Claude Henquin's lab, University of Louvain, Unit of Endocrinology and Metabolism, Brussels, Belgium. « The oscillations of insulin secretion: triggering by cytosolic calcium and modulation by amplification systems in b cells»
Funding :
- 2022-2025: French National Research Agency (ANR)
- 2020-2023: Société Francophone du Diabète
- 2015: Université de Montpellier
- 2012-2015: French National Research Agency (ANR)
- 2011-2014: Fondation pour la Recherche Médicale (FRM)
- 2010-2012: Société Francophone du Diabète
- 2007-2008: Société Francophone du Diabète
- 2006-2009: FNRS Fellowship
Awards :
- 2011: Rising Star from European Association for the Study of Diabetes.
https://www.easd.org/prizes.html
- 2005: AREDIC (Association pour la Recherche sur le Diabète,
Scientific summary
Pancreatic ß-cells are the unique cells of the organism with the capacity to biosynthesize, store and secrete insulin in response to physiological needs. ß-cells play a central role in the etiology of Diabetes. Preservation or restoration of a functional ß-cell mass is essential. Our objectives, divided into basic research components and clinical investigation, are to examine the cellular and molecular mechanisms controlling function, survival and death of ß-cells, to investigate how these go awry in the pathogenesis of diabetes, and how stress and environnement influence ß-cell function and survival.
A better understanding of the signaling pathways linked to G-protein coupled receptors (GPCRs) and tyrosine kinase receptors (TKRs) in ß-cells is essential to identify new molecular targets to treat Diabetes with the aim to preserve or restore the functional ß-cell mass.
My specific aims are to identify the cellular and molecular mechanisms involved in the synergism between signaling pathways engaged by GPCRs (GLP-1 and GIP receptors, taken as drug targets for type 2 diabetes), TKRs (Insulin and IGF-1 receptors) and glucose in ß-cells.
