Proceedings of The Physiological Society

University of Oxford (2011) Proc Physiol Soc 23, C10

Oral Communications

Maternal Dietary High Fat Impairs Vascular Function in Offspring

C. J. Kelsall1, N. A. Irvine1, C. Torrens1, K. A. Lillycrop2, M. A. Hanson1, P. C. Calder1, G. C. Burdge1

1. Faculty of Medicine, University of Southampton, Southampton, Hampshire, United Kingdom. 2. Faculty of Natural and Environmental Sciences, University of Southampton, Southampton, Hampshire, United Kingdom.

Human populations exhibit temporal and cross-sectional variations in fatty acid intake. Variations in dietary saturated (SFA), polyunsaturated (PUFA) and trans fatty acid (TFA) intakes altered cardiovascular disease risk in humans1. Maternal high saturated fat diet during pregnancy and lactation in rats is associated with impairment of vascular function in offspring2, but it is not known whether differences in the type of maternal dietary fat influence future cardiovascular function in the offspring. Female rats were fed either 7% (w/w) or 21% (w/w) safflower oil (SAO, enriched in linoleic acid), hydrogenated soybean oil (HSO, enriched inTFA), butter (enriched in SFA) or fish oil (FO, enriched in eicosapentaenoic and docosahexaenoic acids) from two weeks prior to mating until offspring were weaned at day 28 onto AIN93M (4% w/w soybean oil). Endothelial function (relaxation to acetylcholine; ACh, 0.1 nM to 1 μM) was measured ex vivo in thoracic aorta from 77 day old offspring by wire myography. Rat aorta relaxation to ACh is entirely dependent on nitric oxide3, so aortic tissue endothelial nitric oxide synthase (eNOS) mRNA expression was assessed by real-time RT-PCR. Data is % relaxation to ACh, mean ± SD, n = 6 per group. Statistical analysis was performed using a general linear model with Tukey’s post hoc testing, significance being ascribed at p <0.05. There was a significant effect of sex (p 0.027) and total maternal dietary fat (p 0.0001), and an interactive effect of sex and maternal total dietary fat (p 0.04) on ACh-induced relaxation in aorta, but there was no effect of type of maternal dietary fat. Relaxation to 30 nM ACh was impaired in male offspring of dams fed 21% SAO (0.5 ± 5.8), HSO (1.8 ± 15.5) or FO (6.1 ± 13.5), but not butter, compared to offspring of 7% dams (SAO 32.4 ± 18.5; HSO 37.6 ± 21.5; FO 46.4 ± 22.4). Relaxation was impaired in female offspring of dams fed 21% SAO (7.3 ± 10.7), butter (17.6 ± 10.3) or FO (7.6 ± 9.6), but not HSO, compared to offspring of 7% dams (SAO 35.9 ± 31.4; Butter 60.2 ± 23.8; FO 53.0 ± 16.0). eNOS expression was not significantly different between any groups. The data show that maternal dietary high fat persistently impairs offspring aorta endothelial function, contingent on sex. This effect is not due to changes in eNOS expression.

Where applicable, experiments conform with Society ethical requirements