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INSULYSOSOME SIGNED

The role of CD63 in lysosomal degradation of insulin granules in pancreatic beta cells in T2D diabetes

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 INSULYSOSOME project word cloud

Explore the words cloud of the INSULYSOSOME project. It provides you a very rough idea of what is the project "INSULYSOSOME" about.

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Project "INSULYSOSOME" data sheet

The following table provides information about the project.

Coordinator
CENTRE EUROPEEN DE RECHERCHE EN BIOLOGIE ET MEDECINE 

Organization address
address: Rue Laurent Fries 1
city: ILLKIRCH GRAFFENSTADEN
postcode: 67404
website: www.igbmc.fr

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country France [FR]
 Total cost 173˙076 €
 EC max contribution 173˙076 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2017
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2018
 Duration (year-month-day) from 2018-11-01   to  2020-10-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    CENTRE EUROPEEN DE RECHERCHE EN BIOLOGIE ET MEDECINE FR (ILLKIRCH GRAFFENSTADEN) coordinator 173˙076.00

Map

 Project objective

The pancreatic β cell harbors an exemplary nutrient sensing machinery that is coupled to secretion of insulin. While mechanisms governing regulation of insulin secretion in response to nutrients were widely investigated, little is known about how nutrients impact on other basic cellular processes such as insulin granule turnover, autophagy and cellular growth, deregulation of all of which have been demonstrated to be involved in β cell failure in type 2 diabetes (T2D). T2D represents a major health burden accounting for a large part of exploding health costs world-wide. Restoring normal weight through exercise and decreased food consumption in principle is straight-forward to mitigate metabolic disturbances. However, changing the sedentary life style is very challenging for obese subjects and that at a late disease stage, β cell failure becomes irreversible. There is an emerging endeavor of the pharmaceutical industry to develop strategies targeting the β cell that go beyond improving insulin secretion. A prevailing concept in cell biology is that enhanced degradation of cellular components through autophagy can counteract energy depletion caused by shortage of environmental nutrients. My host laboratory recently discovered that β cells employ a very distinct and so far unknown mechanism to adapt to nutrient depletion. β cells induce specific degradation of newly formed insulin granules through lysosomes and suppress autophagy upon nutrient withdrawal. Insulin granule degradation allows for generation of intracellular nutrients and in the same time avoids release of these granules. Their preliminary results suggest that lysosomal insulin granule degradation is dramatically enhanced in β cells of diabetic islets from mice and humans. This increase is accompanied by a drop in autophagy, a known protective process in the β cell. My project will fortify that impaired lysosomal activity, insulin degradation and suppressed autophagy contribute to β cell failure in T2D.

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The information about "INSULYSOSOME" are provided by the European Opendata Portal: CORDIS opendata.

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