Biopharmacy Cell therapy Home_Spotlight — 30 November 2012
Prestigious European Albert Renold Award granted to Professor Decio L. Eizirik of the Universite Libre de Bruxelles (ULB).

Dr. Decio L. Eizirik, Laboratory Director
and Professor at the Medical Faculty, Université Libre de Bruxelles (ULB), since 2002, has been selected for the 2012 Albert Renold Prize by the European Association for the Study of Diabetes (EASD).

Considered to be the most important international prize to be awarded in the field of pancreatic islets, the award recognizes an individual for their outstanding contribution to the advancement of knowledge and research in the field of islets of Langerhans*.

Professor Eizirik directs the Laboratory of Experimental Medicine (ULB) where he is currently heading a team of 27 researchers and laboratory assistants focused on pancreatic beta cell dysfunction and death in diabetes. Through supportive grants received from the FNRS, Biowin and Action Research Initiatives (Federation Wallonia-Brussels); the European Community (projects BetaImage, BetaBat and Naimit); and the American Foundation JDRF, he and his colleagues have been investigating the molecular pathways involved in immune-induced beta cell impairment and apoptosis (programmed cell death), in Type 1 Diabetes (T1D).

T1D is the result of the autoimmune destruction of the vitally important pancreatic beta cells whose primary function is to store and release insulin. In other words, T1D is caused by an autoimmune response where one’s own immune system attacks the beta cells and eventually destroys them. As a result, the body no longer has the ability produce and secrete insulin into the blood and therefore is unable to regulate the blood glucose concentration. As a consequence, T1D patients depend on several daily injections of insulin to maintain adequate blood glucose.

Dr. Eizirik’s award-winning investigative research has shown that several candidate genes for T1D play an important role at the beta cell level and in fact, interact with environmental signals such as viral infections. His research has led to fundamental concepts such as the communication between the body’s immune system and the beta cells that trigger and amplify islet inflammation (insulitis) and progressive beta cell death by apoptosis. For example, by using functional genomics and bioinformatic tools, he and his group have identified certain cytokine-regulated gene networks that define the beta cell outcome following immune-mediated damage. This led to the recent discoveries of the role of endoplasmic reticulum stress and alternative splicing in this process; and the identification of the mitochondrial pathways that ultimately trigger beta cell apoptosis.

By proposing that the beta cell is an active player in processes leading to its survival or death in T1D, he changed the prevailing view in the field and identified several potential targets for therapy aiming at protecting beta cells in early diabetes. He is now pursuing novel alternatives to prevent beta cell death in diabetes, and searching for safe approaches to deliver the protective molecules to the beta cells.

Good luck to Professor Eizirik and his team for their continued efforts on developing the novel approaches to prevent beta-cell death in early diabetes, and congratulations to another Belgian recipient on receiving such a prestigious international award.

* clusters of pancreatic endocrine cells that sense blood sugar levels and release insulin to maintain normal levels.

 Professor Eizirik’s list of distinguished awards and contributions include: the Career Development Award from the Juvenile Diabetes Research Foundation International (JDRFI), the Research Prize Pharmacia & Upjohn (Belgium), the JDRFI Diabetes Care Research Award, the Trondheim Honorary Lecture and more than 270 scientific publications (h-index of 59).



Decio L. Eizirik, M.D., Ph.D.
Professor and Director, Laboratory of Experimental Medicine
Université Libre de Bruxelles (ULB)
808 Route de Lennik
B-1070 Brussels, Belgium

Tel:  32 2 555 62 42
Fax: 32 2 555 62 39








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