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Submitted on June 21, 2005
Accepted on September 23, 2005
School of Anatomy and Human Biology, The University of Western Australia, Nedlands, Perth, Western Australia 6009, Australia; School of Medicine and Pharmacology, Royal Perth Hospital Unit, The University of Western Australia, Medical Research Foundation Building, Perth, Western Australia 6001, Australia
* To whom correspondence should be addressed. E-mail: bwaddell{at}anhb.uwa.edu.au.
Fetal programing is now recognized as a key determinant of the adult phenotype, with major implications for adult-onset diseases including hypertension. Two mediators of fetal programing are maternal nutrition and fetal glucocorticoid exposure. Recent studies show that postnatal dietary manipulations can exacerbate programing effects, but whether programing effects can be attenuated by postnatal dietary manipulations, and thus provide a possible therapeutic strategy, is unknown. In this study we tested the hypothesis that a postnatal diet enriched with long chain omega-3 fatty acids attenuates programed hyperleptinemia and hypertension. Pregnant rats were treated with dexamethasone from day 13 to term and offspring were cross-fostered to mothers on either a standard diet or a diet high in omega-3 fatty acids, and remained on these diets post-weaning. Maternal dexamethasone reduced birthweight and delayed the onset of puberty in offspring. Hyperleptinemia (associated with elevated leptin mRNA expression in adipose tissue) and hypertension were evident in offspring by 6 months of age in dexamethasone-exposed animals consuming a standard diet, but these effects were completely blocked by a high omega-3 diet. These results demonstrate for the first time that manipulation of postnatal diet can limit adverse outcomes of fetal programing, with programed hyperleptinemia and hypertension prevented by a postnatal diet enriched with omega-3 fatty acids. This raises the possibility that dietary supplementation with omega-3 fatty acids may provide a viable therapeutic option for preventing and/ or reducing adverse programing outcomes in humans.
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