Spotlight on Research: Dr. Jean Buteau

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Diabetes mellitus is characterized by insufficient production of insulin by the pancreas, resulting in hyperglycemia. In the pancreas, insulin is produced by specialized cells called “beta-cells”, which have long attracted the interest of Dr. Jean Buteau.

Dr. Buteau received a PhD in Biochemistry from Université de Montréal. His PhD thesis investigated the action of Glucagon-Like Peptide-1 (GLP-1), a naturally-occurring hormone secreted by the small intestine that possesses several glucose-lowering properties. As such, GLP-1 and its analogs have been subject to intensive investigation as anti-diabetes medications. Dr. Buteau was one of the first investigators to demonstrate the effects of GLP-1 on pancreatic beta-cell proliferation and survival, revealing a previously unrecognized mode of action of this new class of anti-diabetes medications. Dr. Buteau also worked as a Postdoctoral Fellow at Columbia University in New York City, where he investigated the link between insulin resistance and the deterioration of pancreatic beta-cells. In particular, his work highlighted the role of a protein called Foxo1 in this process.  Throughout his training, Dr. Buteau received several honours and published high-impact publications.

Since 2008, Dr Buteau has been appointed as an Assistant Professor in the Department of Medicine of Université Laval in Quebec City, with support from a Scholar Award from the Canadian Diabetes Association. His current research efforts are aimed at identifying novel genes that regulate beta-cell birth, life and death. The overall goal of his research program is to harness the therapeutic potential of these newly discovered targets to stimulate the generation of new beta-cells and to expand and protect the functional beta-cells that still reside in the pancreas of patients with diabetes.

In his most recent publication, Dr. Buteau used a combination of beta-cell lines, primary human beta-cells and transgenic mice to investigate the role of a protein called SirT1 in beta-cells. His multidisciplinary approach using genetic, pharmacological and biochemical analyses suggested that SirT1 could act as a negative regulator of beta-cell expansion. This work was published in the journal Diabetes.

Dr. Buteau’s work could lead to the identification of novel pharmacological targets that could have a clinical benefit for most patients with diabetes. “The more we know about the mechanisms that regulate beta-cell birth, life and death; the better we will be able to treat type 1 and type 2 diabetes” says Dr. Buteau.