BCELL-T2D

Role of pancreatic beta-cell regeneration in the pathofisiology and treatment of insulin resistance and type 2 diabetes

 Coordinatore Fundación para la Gestión de la Investigación Biomédica de Cádiz 

 Organization address city: CADIZ
postcode: 11009

contact info
Titolo: Ms.
Nome: Diana
Cognome: Regueiro
Email: send email
Telefono: 34956245019
Fax: 34956002347

 Nazionalità Coordinatore Spain [ES]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2009-RG
 Funding Scheme MC-IRG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-10-01   -   2014-01-20

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    Nome Ente NON disponibile

 Organization address city: CADIZ
postcode: 11009

contact info
Titolo: Ms.
Nome: Diana
Cognome: Regueiro
Email: send email
Telefono: 34956245019
Fax: 34956002347

ES (CADIZ) coordinator 100˙000.00

Mappa


 Word cloud

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

compensate    cell    mechanisms    decrease    cells    develops    health    mice    cycle    diabetes    pancreatic    epidemic    beta    cyclin    molecular    tolerance    insulin    proliferation    techniques    glucose    db    identification    resistance    therapeutic   

 Obiettivo del progetto (Objective)

'Diabetes is a devastating illness declared by the World Health Organization as the XXI century epidemic. It is urgent to define the factors contributing to diabetes onset and severity, and to identify new potential therapies to prevent and treat diabetes and its complications. Type 2 diabetes develops through a multi-stage process. The body becomes unable to use insulin effectively and the pancreatic beta cells try to compensate producing more insulin, a condition known as insulin resistance. Eventually the beta cells become exhausted and cannot produce enough insulin to overcome insulin resistance. At this point, this condition frequently progresses to diabetes. Diabetes develops after a substantial decrease in the number of beta cells (increase in cell death/decrease in proliferation and neogenesis) and/or the impairment of insulin secretion needed to maintain euglycemia. The molecular mechanisms by which beta cells fail to compensate for insulin resistance remain elusive. The aims are: 1) Identification of the molecular mechanisms that lead to impaired beta cell proliferation in the pathophysiology of type 2 diabetes. 2) Therapeutic role of beta-cell proliferation in the treatment of type 2 diabetes. To address aim 1, db/db mice deficient for the leptin receptor on a C57BLKS/J background (a genetic model of obesity that develops diabetes) will be used. The techniques chosen for this aim include: proliferation studies; identification and quantification of cell cycle control proteins (western-blot, RT-PCR and immunofluorescence); techniques to study glucose/insulin homeostasis (glucose/insulin levels, glucose tolerance test and insulin tolerance test). To address aim 2, adenoviral vectors that contain cDNA of cell cycle activators (cyclin C, cyclin D1, D2, D3, cyclin E and their associated kinases cdk-3, -4 and -2) will be injected through the pancreatic duct in mice prone to develop diabetes (as in aim 1). The techniques will be similar to the ones in aim'

Introduzione (Teaser)

Diabetes constitutes a serious global health issue that has reached epidemic proportions over the past years. Understanding how the disease develops will help identify potential therapeutic targets.

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