Dietary protein restriction in the pregnant rat induces altered epigenetic regulation of the glucocorticoid receptor and peroxisomal proliferator-activated receptor alpha in the heart of the offspring which is prevented by folic acid.


Lillycrop, K.A., Phillips, E.S., Jackson, A.A., Hanson, M.A. and Burdge, G.C. (2006) Dietary protein restriction in the pregnant rat induces altered epigenetic regulation of the glucocorticoid receptor and peroxisomal proliferator-activated receptor alpha in the heart of the offspring which is prevented by folic acid. Proceedings of the Nutrition Society, 65, (OCA-B), p.65A. (doi:10.1017/S002966510600526X).

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Description/Abstract

In healthy individuals, glucose and fatty acids are substrates for ATP generation in the heart. There is emerging evidence from patients with type 2 diabetes mellitus that preferential use of fatty acid b-oxidation for energy production may be linked to cardiomyopathy (Fink, 2004). PPARa activity is important for regulating fatty acid b-oxidation in the heart and is increased in hearts of rats with experimentally induced diabetes (Fink, 2004). Prenatal undernutrition is related inversely to risk of type 2 diabetes mellitus in man (Poole & Byrne, 2005) and insulin resistance in rats (Bertram & Hanson, 2001). We have shown that maternal dietary protein restriction induces persistent alterations to hepatic and carbohydrate metabolism in the offspring by altering the epigenetic regulation of PPARa and the glucocorticoid receptor (GR) (Lillycrop et al. 2005). Here we have tested the hypothesis that prenatal protein restriction induces hypomethylation of the GR and PPARa promoters in the heart, and that this is prevented by supplementation of the protein-restricted (PR) diet with folic acid.

Item Type: Article
Digital Object Identifier (DOI): doi:10.1017/S002966510600526X
ISSNs: 0029-6651 (print)
Subjects:
ePrint ID: 56173
Date :
Date Event
1 January 2006Published
Date Deposited: 11 Aug 2008
Last Modified: 16 Apr 2017 17:41
Further Information:Google Scholar
URI: http://eprints.soton.ac.uk/id/eprint/56173

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