INSIGHT

An Integrated Network of Glucose Sensing Cells in Glucose Homeostasis

 Coordinatore UNIVERSITE DE LAUSANNE 

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 Nazionalità Coordinatore Switzerland [CH]
 Totale costo 2˙499˙421 €
 EC contributo 2˙499˙421 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2010-AdG_20100317
 Funding Scheme ERC-AG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-08-01   -   2016-07-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITE DE LAUSANNE

 Organization address city: LAUSANNE
postcode: 1015

contact info
Titolo: Ms.
Nome: Danielle
Cognome: Canepa Del Canto-Perri
Email: send email
Telefono: +41 21 6923980
Fax: +41 21 6923985

CH (LAUSANNE) hostInstitution 2˙499˙421.00
2    UNIVERSITE DE LAUSANNE

 Organization address city: LAUSANNE
postcode: 1015

contact info
Titolo: Prof.
Nome: Bernard Marie
Cognome: Thorens
Email: send email
Telefono: +41 21 6923981
Fax: +41 21 6923985

CH (LAUSANNE) hostInstitution 2˙499˙421.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

glucose    homeostasis    glp    cell    sensing    expenditure    secretion    identification    disease    energy    insulin    glucagon    genetic    genomic    cells    diabetes    molecular    beta    nervous    feeding    pancreatic   

 Obiettivo del progetto (Objective)

'Glucose sensing cells constantly monitor glucose absorption from food and variations in blood glycemic levels. They control the secretion of GLP-1, insulin and glucagon, and the activity of the autonomic nervous system. These hormonal and nervous signals coordinate glucose utilization by liver, fat and muscle, and endogenous glucose production as well as feeding and energy expenditure. Type 2 diabetes, a disease that afflicts an increasing proportion of the world population, is characterized by insufficient insulin production by pancreatic beta-cells, abnormal secretion of GLP-1 and glucagon, and is often associated with imbalance between feeding and energy expenditure. Type 2 diabetes can thus be considered a disease of glucose sensing. Here, I propose a research program using cell biological, genetic, genomic and physiology techniques to investigate three aspects of this integrated glucose sensing network: 1. The identification of novel molecular pathways activated by GLP-1 and that control adult beta-cell proliferation, glucose competence and apoptosis in order to maintain sufficient insulin secretion capacity. 2. The identification and molecular characterization of brain glucose sensors, which share functional similarities with pancreatic beta-cells, and which control glucose homeostasis and pancreatic islet mass and function. 3. The discovery by unbiased genetic-genomic analysis of loci, genes, and gene networks involved in central hypoglycemia detection and the secretion of glucagon, a process whose deregulation is a major limitation in insulin treatment of both type 1 and type 2 diabetes. Together these investigations will bring new knowledge on the integrated control of glucose homeostasis that may lead to novel strategies to control diabetes.'

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