IRBETAINE-CIG

Molecular mechanisms underlying the development of insulin resistance: role of betaine supplementation

 Coordinatore FUNDACIO SANT JOAN DE DEU 

 Organization address address: Calle Santa Rosa
city: Esplugues de Ll
postcode: 8950

contact info
Titolo: Mrs.
Nome: Roser
Cognome: Arnalte
Email: send email
Telefono: 34936009751

 Nazionalità Coordinatore Spain [ES]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 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-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-09-01   -   2015-08-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    FUNDACIO SANT JOAN DE DEU

 Organization address address: Calle Santa Rosa
city: Esplugues de Ll
postcode: 8950

contact info
Titolo: Mrs.
Nome: Roser
Cognome: Arnalte
Email: send email
Telefono: 34936009751

ES (Esplugues de Ll) coordinator 53˙158.60
2    CONSORCI INSTITUT D'INVESTIGACIONS BIOMEDIQUES AUGUST PI I SUNYER

 Organization address address: CALLE ROSSELLO 149 PUERTA BJS
city: BARCELONA
postcode: 8036

contact info
Titolo: Ms.
Nome: Sara
Cognome: Hurst
Email: send email
Telefono: +34 93 227 5707

ES (BARCELONA) participant 46˙841.40

Mappa


 Word cloud

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sensitivity    body    fat    diet    prevention    therapeutic    model    muscle    insulin    risk    humans    mechanisms    supplementation    first    betaine    strategies       mouse    molecular    resistance    induced   

 Obiettivo del progetto (Objective)

'Type 2 diabetes (T2D) is a growing global epidemic and new prevention and therapeutic strategies are urgently needed. Insulin resistance is present in high-risk individuals years before the onset of T2D, making the characterization of the complex pathophysiology of insulin resistance a key element of future prevention efforts. The overall goal of our project is to identify and characterize novel molecular mechanisms underlying the development of insulin resistance to find specific targets for prevention and therapeutic strategies.

Our analysis of the plasma metabolome of humans at risk for T2D suggests that reductions in betaine levels can contribute to insulin resistance. Consistent with this hypothesis, preliminary studies show that betaine supplementation improves insulin sensitivity and whole-body energy expenditure in a mouse model of diet-induced obesity.

First, we propose to determine the mechanisms mediating the beneficial effects of betaine on insulin sensitivity in a diet-induced obese mouse model. For this purpose, C57BL/6 mice will be fed either chow or high-fat diet with or without betaine supplementation. Whole-body and tissue-specific betaine effects will be analyzed to characterize the mechanisms of betaine action. Second, we will apply next generation sequencing of mRNA to analyze the muscle transcriptome associated with high fat feeding and betaine supplementation. As metabolic and molecular changes induced by betaine will be intimately linked to insulin sensitivity, this technique will identify novel genes, alternative splicing isoforms and pathways potentially involved in the development of muscle insulin resistance.

This project will constitute a critical first step for future studies aimed at determining whether betaine supplementation is effective in preventing insulin resistance and progression to T2D in humans. Furthermore, it will identify novel targets for designing prevention and therapeutic strategies for the development of T2D.'

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