META-GROWTH

Metabolic regulation of growth and body composition: key modulators of long-term health

 Coordinatore LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN 

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 Nazionalità Coordinatore Germany [DE]
 Totale costo 2˙491˙200 €
 EC contributo 2˙491˙200 €
 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-2012-ADG_20120314
 Funding Scheme ERC-AG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-10-01   -   2018-09-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
city: MUENCHEN
postcode: 80539

contact info
Titolo: Ms.
Nome: Dorothee
Cognome: Hasebrink
Email: send email
Telefono: +49 89 2180 3605
Fax: +49 89 2180 2985

DE (MUENCHEN) hostInstitution 2˙491˙200.00
2    LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
city: MUENCHEN
postcode: 80539

contact info
Titolo: Prof.
Nome: Berthold
Cognome: Koletzko
Email: send email
Telefono: +49 89 5160 2826
Fax: +49 89 5160 7742

DE (MUENCHEN) hostInstitution 2˙491˙200.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

persistent    childhood    weight    body    nutrient    composition    pregnancy    formula    epigenetic    time    methylation    induce    gain    health    dna    periods    obesity    metabolomic    scientific    acids    metabolic   

 Obiettivo del progetto (Objective)

'Nutrient exposure during pregnancy and childhood strongly affects growth and induces persistent metabolic programming of lifelong health. Recent data show that obesity and related disorders are induced by both fast childhood weight gain, and by formula feeding that promotes higher weight gain than breastfeeding. Lower protein in infant formula at levels similar to breast milk normalizes early weight gain and reduces later obesity risk as much as 2.5fold. Optimizing growth through improved substrate supply is of major importance for health prevention, but information is lacking on key mediators, effects on body composition and mechanisms of action, e.g. epigenetic modification. We use innovative approaches to identify key substrates that may mediate growth and body composition in humans, e.g. branched chain amino acids, n-6 polyunsaturated fatty acids, and others, and their epigenetic effects. We employ novel methods for high throughput targeted metabolomic and lipidomic profiling, genome-wide DNA methylation analysis, and state of the art bioinformatics. These powerful tools are applied to five well designed prospective cohort studies covering critical time periods from pregnancy to puberty. All cohorts offer precise phenotyping incl. body composition and are already or will be established. Comparative analyses across studies and populations provide added scientific value. We will identify which metabolic signals induce rapid weight gain and body fat deposition throughout childhood. We aim at identifying susceptible age periods, nutrient effects on epigenetic DNA methylation, and whether early metabolic exposures induce persistent or fluid metabolomic and epigenetic changes over time. The results should provide answers to key questions on the regulation of growth, with major benefit for scientific understanding, opportunities for future research, promotion of public health, nutrition recommendations, and development of improved food products.'

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