PHD-OB-T2D

STUDY THE ROLE OF OXYGEN SENSORS PROLYL HYDROXYLASE DOMAIN (PHD) PROTEIN IN OBESITY AND TYPE II DIABETES

Coordinatore	VIB    more  Organization address address: Rijvisschestraat 120 city: ZWIJNAARDE - GENT postcode: 9052 contact info Titolo: Dr. Nome: Rik Cognome: Audenaert Email: send email Telefono: 3292446611 Fax: 3292446699
Nazionalità Coordinatore	Belgium [BE]
Totale costo	164˙886 €
EC contributo	164˙886 €
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-2007-2-1-IEF
Funding Scheme	MC-IEF
Anno di inizio	2008
Periodo (anno-mese-giorno)	2008-03-01   -   2010-02-28

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	VIB  Organization address address: Rijvisschestraat 120 city: ZWIJNAARDE - GENT postcode: 9052 contact info Titolo: Dr. Nome: Rik Cognome: Audenaert Email: send email Telefono: 3292446611 Fax: 3292446699	BE (ZWIJNAARDE - GENT)	coordinator	0.00

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 Obiettivo del progetto (Objective)

'Various alterations of metabolism are a central characteristic of physiological disorders and diseases, including cancer, obesity, type 2 diabetes (T2D) and the metabolic syndrome (MS) and are as such a major burden on national budgets. Thus, there is an urgent need to further understand the various processes that determine the occurence of metabolic alterations, predominantly obesity and T2D and to develop strategies to provide therapeutic aid. Several intrinsic factors either predetermine or correlate with the occurence of obesity and the development of T2D and MS. Our laboratory has recently reported a yet unidentified role of the mammalian oxygen sensor PHD1 in the control of glucose homeostasis by phenotyping PHD1 knockout mice. In detail, loss of PHD1 lowers oxygen consumption in skeletal muscle by shifting glucose metabolism from oxidative to more anaerobic ATP production which impairs oxidative muscle performance in healthy conditions, but induces hypoxia tolerance and protects myofibers against lethal ischemia. In addition, novel findings suggest a correlation between PHD1 and intrinsic obesity and T2D related factors. To extend our studies on PHD specific metabolic alterations we will utilize several in the lab made transgenic PHD mice to address the followong issues (i) assess obesity and T2D related changes in lipid and glucose homeostasis in mice lacking each of the PHDs either constitutively or specifically in key metabolic tissues by comparing various metabolic parameters before and after administration of a high fat diet (ii) determine the consequences of loss of PHD function in pancreatic ß-cell physiology, insulin signalling and glucose tolerance using a mouse model of dietary induced diabetes and (iii) determine whether loss of PHD function might have any potential for pharmaceutical intervention by intercrossing our PHD deficient mouse strains with well established mouse models to study obesity and obesity related disorders such as T2D and MS.'