DKK3 T2DM

Wnt agonist Dickkopf 3 (DKK3) is a type 2 diabetes susceptibility gene

 Coordinatore KAROLINSKA INSTITUTET 

 Organization address address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177

contact info
Titolo: Prof.
Nome: Per-Olof
Cognome: Berggren
Email: send email
Telefono: +46 8 517 757 31
Fax: +46 8 517 794 50

 Nazionalità Coordinatore Sweden [SE]
 Totale costo 75˙000 €
 EC contributo 75˙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-2010-RG
 Funding Scheme MC-IRG
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-09-01   -   2013-08-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KAROLINSKA INSTITUTET

 Organization address address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177

contact info
Titolo: Prof.
Nome: Per-Olof
Cognome: Berggren
Email: send email
Telefono: +46 8 517 757 31
Fax: +46 8 517 794 50

SE (STOCKHOLM) coordinator 75˙000.00

Mappa


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pancreatic    islets    allele    canonical       dm    expression    dkk    islet    susceptibility    wnt    cells    impaired    signaling   

 Obiettivo del progetto (Objective)

'Type 2 diabetes mellitus (T2DM) is a complex genetic disorder of largely obscure etiology where alleles at numerous loci are thought to interact with environmental and stochastic cues to induce the phenotype. We have recently identified a T2DM susceptibility allele at the DKK3 locus. Using a combination of case/control association and functional studies, we demonstrated that the minor allele of SNP rs11022111 in the DKK3 promoter is significantly associated with T2DM in two Chinese and one Caucasian cohort and results in the disruption of a conserved SP1 binding site, leading to reduced DKK3 expression. We also showed that, in contrast to other members of the DKK family, DKK3 is a likely agonist of Wnt signaling (both canonical and non-canonical), in a Fz- and LRP6-dependent manner and regulates the expression of TCF7L2, another T2DM susceptibility gene. Our preliminary data implicate the regulation of Wnt signaling in the pathogenesis of T2DM. In this proposal, we hypothesize that aberrant Wnt signaling in the adult pancreas can lead to impaired glucose tolerance, insulin secretion and other diabetic phenotypes. To address how Dickkopf 3 influences Wnt signaling in β-cells and pancreatic islets as well as pancreatic islet functions, I propose to identify the subset of Wnt signaling components that are active in MIN6 cells and islets, to characterize the effect of impaired Wnt signaling on islet function and formation, and finally, to investigate the metabolic state of Dkk3-/- mice when challenged with a high fat diet.'

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