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Roberto Coppari

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Prof. Roberto Coppari

Coordinateur CFD - Métabolisme du cancer et du diabète

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Roberto Coppari is Professor at the Faculty of Medicine of the University of Geneva in Switzerland where he also directs the Faculty Diabetes Center (since 2015) and the Metabolic Core facility (since 2017). Prof. Coppari has been using genetically-engineered mice to dissect the neuronal and peripheral mechanisms underlying glucose, lipid, and energy balance in health and disease (e.g. diabetes). His work aims at understanding how insulin-deficiency-induced lethality can be overcome without the need of injected insulin. Prof. Coppari is also interested in understanding how metabolic pressure (e.g. hyper-caloric feeding) affects cancer cell behavior and cancer stem-like features. His research unraveled new putative targets for treatment of metabolic and cancerous diseases (e.g. FKBP10, PTPRg) and pathways permitting life without insulin (e.g. leptin and its downstream effectors as for example S100A9). Prof. Coppari received a PhD in Neuroscience in 2002 and performed his pre-graduate and post-graduate training at Harvard Medical School in Boston, MA, USA. His independent career started in 2007 when he was appointed Assistant Professor at the University of Texas Southwestern Medical School in Dallas, TX, USA where he worked until the end of 2012. His research was and/or has been funded by several agencies as for example the European Research Council (e.g. ERC consolidator, ERC Proof of Concept grants), the USA National Institutes of Health (e.g. RO1 grants), the Swiss Cancer League, the Juvenile Diabetes Research Foundation and the Swiss National Science Foundation. Prof. Coppari has organized several national and international meetings and is a member of the Direction Committee of the Lausanne Integrative Metabolism and Nutrition Alliance and of the Dean Advisory Board at the Faculty of Medicine, University of Geneva, Switzerland.

Research aims

The Coppari laboratory investigates brain-driven mechanisms that would permit life without insulin. These mechanisms may represent new therapeutic targets for improving diabetes mellitus type 1 (T1DM) and type 2 (T2DM)

  • Identifying neuron-types and molecules underlying normal metabolic homeostasis;
  •  Identifying neuron-types and molecules protecting against diet-induced metabolic imbalance;
  •  Identifying neuron-types and molecules permitting life without insulin;
  • Exploiting effect of dietary interventions to unveil cancer vulnerabilities.

Expertise

  • Generation of genetically-engineered mice bearing neuron-type-restricted mutations;
  •  Metabolic assessments, including glucose/insulin clamp in unrestrained and awake rodents;
  • Dietary interventions affecting cancer biology in rodents.

 

More information on Prof. Coppari's reserach and recent publications on his group website.

 


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