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Prevention of diet‐induced obesity by apple polyphenols in W istar rats through regulation of adipocyte gene expression and DNA methylation patterns

This study was conducted to determine the mechanisms implicated in the beneficial effects of apple polyphenols ( AP s) against diet‐induced obesity in W istar rats, described in a previous study from our group. Supplementation of high‐fat sucrose diet with AP prevented adiposity increase by inhibiti...

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Published in:Molecular nutrition & food research 2013-08, Vol.57 (8), p.1473-1478
Main Authors: Boqué, Noemi, de la Iglesia, Rocío, de la Garza, Ana L., Milagro, Fermín I., Olivares, Mónica, Bañuelos, Óscar, Soria, Ana Cristina, Rodríguez‐Sánchez, Sonia, Martínez, José Alfredo, Campión, Javier
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Language:English
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Summary:This study was conducted to determine the mechanisms implicated in the beneficial effects of apple polyphenols ( AP s) against diet‐induced obesity in W istar rats, described in a previous study from our group. Supplementation of high‐fat sucrose diet with AP prevented adiposity increase by inhibition of adipocyte hypertrophy. Rats supplemented with AP exhibited improved glucose tolerance while adipocytes isolated from these rats showed an enhanced lipolytic response to isoproterenol. AP intake led to reduced L ep , P lin , and sterol regulatory element binding transcription factor 1 ( S rebf1 ) m RNA levels and increased aquaporin 7 ( A qp7 ), adipocyte enhancer binding protein 1 ( A ebp1 ), and peroxisome proliferator‐activated receptor gamma co‐activator 1 alpha ( Ppargc1a ) m RNA levels in epididymal adipocytes. In addition, we found different methylation patterns of A qp7 , L ep , P pargc1a , and S rebf1 promoters in adipocytes from apple‐supplemented rats compared to high‐fat sucrose fed rats. The administration of AP protects against body weight gain and fat deposition and improves glucose tolerance in rats. We propose that AP exerts the antiobesity effects through the regulation of genes involved in adipogenesis, lipolysis, and fatty acid oxidation, in a process that could be mediated in part by epigenetic mechanisms.
ISSN:1613-4125
1613-4133
DOI:10.1002/mnfr.201200686