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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.

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

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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