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GLIODIABESITY SIGNED

ROLE OF THE TANYCYTIC BARRIER AT THE BLOOD-HYPOTHALAMUS INTERFACE DURING METABOLIC DISORDER DEVELOPMENT

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 GLIODIABESITY project word cloud

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

clinical    boosting    sites    cerebrospinal    hypothalamic    strengthen    regulate    genetically    career    circulating    adiposity    critical    periphery    convey    death    humans    barrier    diet    vivo    molecular    pathophysiology    responsible    obese    scientific    tanycytes    mice    neural    collaborations    alteration    proportion    expenditure    formative    hypothalamus    homeostasis    conduit    laboratory    energy    lining    transport    administration    insulin    mechanism    expand    underlying    fail    signals    contents    modified    networks    hold    anticipated    closer    reduce    age    appetite    csf    hyperphagia    human    diabetes    shuttling    fat    treating    fluid    combination    deficient    solid    barriers    demonstrated    display    reduces    mechanisms    resistance    blood    paving    paradoxically    action    besides    host    endowed    models    borne    defective    patients    limiting    metabolic    disorders    brain    diseases    body    blunted    leptin    elucidate    play    glia    vitro    raises    therapeutic    onset    obesity    levels    floor    possibility    ventricle   

Project "GLIODIABESITY" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITE DE LILLE II - DROIT ET SANTE 

There are not information about this coordinator. Please contact Fabio for more information, thanks.

 Coordinator Country France [FR]
 Project website http://hypothalamus.eu/
 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-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2015
 Duration (year-month-day) from 2015-07-01   to  2017-06-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITE DE LILLE FR (LILLE) coordinator 173˙076.00
2    UNIVERSITE DE LILLE II - DROIT ET SANTE FR (Lille) coordinator 0.00

Map

 Project objective

Metabolic disorders such as obesity and diabetes are age-related diseases, and lead cause of death in Europe. Adiposity signals such as leptin and insulin, whose circulating levels are in proportion to body fat, convey metabolic information to neural networks that regulate energy homeostasis in the hypothalamus. In leptin-deficient humans and mice, leptin administration effectively reduces hyperphagia and obesity. Paradoxically, most cases of obesity display high circulating leptin levels that fail to reduce appetite or increase energy expenditure. This raises the possibility that leptin transport across the blood-brain barrier to the cerebrospinal fluid (CSF) or to its sites of action within the hypothalamus is a limiting step defective in obese patients. The host laboratory recently demonstrated that tanycytes, a hypothalamic glia lining the floor of the third ventricle, were responsible for shuttling leptin from the periphery to the CSF and that such conduit was blunted in mice with diet-induced obesity. Leptin transport by tanycytes could thus play a critical role in the pathophysiology of leptin resistance. The overall objective of this project is to further elucidate whether the alteration of the adiposity signals transport into the metabolic brain across hypothalamic barriers is the main cause of the onset of obesity. To this end, a combination of in vitro and in vivo approaches, using genetically modified mice and pre-clinical models of obesity, will be implemented in order to elucidate the molecular mechanisms for the transport of blood-borne leptin into the CSF by tanycytes. It is anticipated that implementation of this project will expand our knowledge of the mechanism underlying human obesity and hold therapeutic potential for treating it. Besides, the proposed project is endowed of solid formative contents that will strengthen the experience of the applicant, boosting her future scientific career and paving the way for closer scientific collaborations.

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

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