MULTI-ISLET

Development of Multiscale Analysis of Pancreatic Beta-Cell Function by Imaging Islets in situ within the Intact Pancreas

Coordinatore	IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE    more  Organization address address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD city: LONDON postcode: SW7 2AZ contact info Titolo: Ms. Nome: Tatjana Cognome: Palalic Email: send email Telefono: +44 207 594 3866
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	200˙371 €
EC contributo	200˙371 €
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-2011-IEF
Funding Scheme	MC-IEF
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-03-01   -   2014-02-28

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE  Organization address address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD city: LONDON postcode: SW7 2AZ contact info Titolo: Ms. Nome: Tatjana Cognome: Palalic Email: send email Telefono: +44 207 594 3866	UK (LONDON)	coordinator	200˙371.80

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 Obiettivo del progetto (Objective)

'Type 2 diabetes is a global and costly healthcare problem associated with impaired insulin secretion from pancreatic beta-cells as well as peripheral insulin resistance. The range of complications associated with aberrant glucose homeostasis is vast, and some severely impact the ability of diabetes-sufferers to lead a normal life. Despite significant research funding over the past three decades, the incidence of diabetes continues to grow. The finding in recent years that genes predispose to diabetes has ignited a search for the mechanisms through which diabetes-associated genes predispose to diabetes. At the single cell level, gene-silencing/transduction studies using cell cultures have shown that gene polymorphisms consistently associated with diabetes, such as those for TCF7L2, lead to defects in insulin processing, storage and secretion. At the whole-animal level, beta-cell specific deletion of TCF7L2 leads to marked glucose intolerance. Yet, directly extrapolating findings between these two levels is complicated by the dependence of beta-cells on their tissue context for proper function. To overcome this obstacle, and adequately reconcile these observations, further studies are required to assess how type 2 diabetes-associated genes alter beta-cell function at the single cell and population levels in the intact tissue. By applying multiphoton imaging and optogenetics to murine models of type 2 diabetes, new insights into the influence of identified risk genes on beta-cell behavior at multiple levels can be obtained. It is hoped that the findings stemming from these studies will allow new therapeutic targets to be identified in the future.'