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GENE TARGET T2D

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General and targeted approaches to unravel the molecular causes of type 2 diabet...

General and targeted approaches to unravel the molecular causes of type 2 diabetes Type 2 diabetes (T2D) affects worldwide at present about 250 million patients and an estimated 380 million in 2025. This epidemic has been ascribed to a collision between genes and an affluent society. Genetics of T2D has during r... ver más

30/04/2016

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

MAX IV Laboratory, Lund University No se ha especificado una descripción o un objeto social para esta compañía.

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2016-04-30 No tenemos la información de la convocatoria

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1 Participantes

2.50M€ | Lider

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Líder del proyecto

MAX IV Laboratory, Lund University No se ha especificado una descripción o un objeto social para esta compañía.

Presupuesto del proyecto 2M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Type 2 diabetes (T2D) affects worldwide at present about 250 million patients and an estimated 380 million in 2025. This epidemic has been ascribed to a collision between genes and an affluent society. Genetics of T2D has during recent years identified > 30 variants increasing susceptibility to T2D. Yet, these variants explain only 15% of the heritability of T2D. One reason could be that whole genome association studies can only detect common variants whereas identification of rare variants with stronger effects would require sequencing. A large part of this application is devoted to sequencing of affected family members from unique large pedigrees traced back to common ancestors around 1600. The advantage of using families is that identified variants can be tested for segregation with the trait. Genetic variants can influence expression of a gene in an allele specific manner. This will be explored by combining exome sequencing with sequencing of RNA from human islets. Impaired effects of the incretin hormones GLP-1 and GIP on the pancreatic islets represent central defects in T2D. Variants in the TCF7L2 and GIPR genes contribute to these defects. I will here explore the molecular mechanisms by which TCF7L2, the strongest T2D gene, causes T2D. GIP has unprecedented effects not only on islet function but also on body composition, blood flow and vascular complications in T2D. This application explores these effects and will test whether manipulation of GIP can mimic the normalization of glucose tolerance seen after gastric bypass surgery. Taken together, these general and targeted approaches are expected not only to provide new insights into the causes of T2D but also contribute with vital information for development of new treatments for T2D.

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