OBERSTRESS

Hypothalamic Lipotoxicity and Endoplasmic Reticulum Stress: a New Pathophysiological Mechanism of Obesity

 Coordinatore UNIVERSIDADE DE SANTIAGO DE COMPOSTELA 

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 Nazionalità Coordinatore Spain [ES]
 Totale costo 1˙484˙000 €
 EC contributo 1˙484˙000 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2011-StG_20101109
 Funding Scheme ERC-SG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-12-01   -   2016-11-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSIDADE DE SANTIAGO DE COMPOSTELA

 Organization address address: "PAZO DE SAN XEROME, PRAZA DO OBRADOIRO S/N"
city: SANTIAGO DE COMPOSTELA
postcode: 15782

contact info
Titolo: Dr.
Nome: Miguel Antonio
Cognome: López Pérez
Email: send email
Telefono: +34 647 344442
Fax: +34 981 574145

ES (SANTIAGO DE COMPOSTELA) hostInstitution 1˙484˙000.00
2    UNIVERSIDADE DE SANTIAGO DE COMPOSTELA

 Organization address address: "PAZO DE SAN XEROME, PRAZA DO OBRADOIRO S/N"
city: SANTIAGO DE COMPOSTELA
postcode: 15782

contact info
Titolo: Mr.
Nome: Martin
Cognome: Cacheiro Martinez
Email: send email
Telefono: +34 881 816233
Fax: +34 881816263

ES (SANTIAGO DE COMPOSTELA) hostInstitution 1˙484˙000.00

Mappa


 Word cloud

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lipotoxicity    er    balance    metabolic    hypothalamus    energy    context    complications    applicant    stress    hypothalamic    mechanisms    chop    determine    obesity   

 Obiettivo del progetto (Objective)

'It is well established that metabolically relevant organs such as adipose tissue, pancreatic beta cells, liver and skeletal muscle develop endoplasmic reticulum (ER) stress under conditions of obesity induced lipotoxicity. Here, the applicant will investigate if/how the hypothalamus is affected by lipotoxicity and ER stress in the context of obesity

* Scientific Hypotheses: 1. Obesity is associated with lipotoxicity and ER stress in the hypothalamus. 2. Hypothalamic ER stress may contribute to the development of obesity through dysregulation of the mechanisms controlling energy balance. 3. Based on our preliminary data, we hypothesize that CHOP, a mediator of ER stress, could be a key modulator of the association between obesity and ER dysfunction in the hypothalamus.

* General Objective: to determine the relevance of hypothalamic lipotoxicity and ER stress for the development of obesity and whether targeting ER stress mechanisms is a successful therapeutic strategy to prevent or revert obesity and its metabolic complications.

* Specific Objectives: 1. To determine whether obesity and the metabolic syndrome are associated with hypothalamic lipotoxicity, ER stress and whether these effects are hypothalamic nuclei specific 2. To determine whether primary hypothalamic ER stress is a cause of altered energy balance leading to obesity and metabolic complications 3. To determine whether in the context of obesity inhibition of ER stress in hypothalamus affects energy balance and obesity associated metabolic complications 4. To determine the role of CHOP on energy balance and obesity in specific hypothalamic neuronal populations

This project is central to the applicant’s goal of understanding how the hypothalamus regulates energy balance under physiological and pathophysiological conditions, as an essential step towards identifying and developing novel molecular drug targets to tackle the problem of obesity and their metabolic complications.'

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