Raised dietary n-6 polyunsaturated fatty acid intake increases 2-series prostaglandin production during labour in the ewe
Elmes, M., Green, L.R., Poore, K., Newman, J., Burrage, D., Abayasekara, D.R.E., Cheng, Z., Hanson, M.A. and Wathes, D.C. (2005) Raised dietary n-6 polyunsaturated fatty acid intake increases 2-series prostaglandin production during labour in the ewe. Journal of Physiology, 562, (2), 583-592. (doi:10.1113/jphysiol.2004.071969).
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Preterm labour is the major cause of perinatal morbidity and mortality in humans. The incidence is around 10% and the causes are often unknown. Consumption of dietary n-6 polyunsaturated fatty acids (PUFAs) in western societies is increasing. These are metabolized to arachidonic acid, the precursor for 2-series prostaglandins (PGs), major signalling molecules during labour. This study investigated the effect of dietary supplementation with linoleic acid (LA, 18: 2, n-6) on parturition. Ewes were fed a control or LA-supplemented diet from 100 days gestation. Labour was induced using a standardized glucocorticoid challenge (dexamethasone, Dex) to the fetus, starting on day 139. Electromyographic (EMG) activity and fetal and maternal circulating PG concentrations were monitored. One third of LA-fed ewes delivered early (pre-Dex) although basal uterine EMG activity preceding Dex was higher in control ewes (P < 0.05). A steep increase in EMG activity occurred 18–38 h after the start of Dex infusion. Twice basal EMG activity (defined as established labour) occurred on average 7 h earlier in the LA-supplemented ewes (P < 0.05). The basal concentrations of maternal and fetal PGFM and fetal PGE2 were approximately doubled in LA-supplemented ewes before the start of Dex infusion (P < 0.01). The rise in fetal PGE2 and maternal oestradiol concentrations post-Dex occurred earlier in the LA-supplemented ewes. All PG measurements remained significantly higher in the LA-supplemented ewes during labour onset. This study suggests that consumption of a high LA diet in late pregnancy can enhance placental PG production and may thus increase the risk of preterm labour.
|Digital Object Identifier (DOI):||doi:10.1113/jphysiol.2004.071969|
|Subjects:||R Medicine > RG Gynecology and obstetrics
Q Science > QP Physiology
|Divisions:||University Structure - Pre August 2011 > School of Medicine > Developmental Origins of Health and Disease
|Date Deposited:||10 Apr 2006|
|Last Modified:||06 Aug 2015 02:25|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
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