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 Nutritional Society, 65, (OCA-B), p.65A. (doi:10.1017/S002966510600526X).
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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.
|Digital Object Identifier (DOI):||doi:10.1017/S002966510600526X|
|Subjects:||Q Science > QH Natural history > QH301 Biology|
|Divisions:||University Structure - Pre August 2011 > School of Biological Sciences
|Date Deposited:||11 Aug 2008|
|Last Modified:||06 Aug 2015 02:45|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
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