The British Journal of Nutrition has accepted our paper entitled ‘Fetal and neonatal exposure to trans fatty acids impacts on susceptibility to atherosclerosis in apolipoprotein E*3 Leiden mice‘, for publication. The study authors are Louise Gates, Simon Langley-Evans, Jana Kraft, Adam Lock and Andy Salter. The work was funded by the United States Department of Agriculture as a collaboration between the universities of Michigan, Vermont and Nottingham, and was an element of Louise Gates PhD studies.
The abstract of the paper is below:
Nutrition during pregnancy impacts on the susceptibility of the offspring to a range of chronic diseases, including cardiovascular disease. Postnatal consumption of trans fatty acids (TFA), associated with partially hydrogenated vegetable oil (P-TFA), has been linked to increased risk of atherosclerosis, while evidence for those trans fatty acids associated with ruminant-derived dairy and meat (R-TFA) remain equivocal. Here, we investigate the impact of maternal consumption of dietary P-TFA and R-TFA on the development of atherosclerosis in their offspring, using the transgenic apoE*3 Leiden mouse. Dams were fed either chow or one of three high fat diets: a high-fat diet designed to reflect the saturated fatty acid content of a ‘Western’ diet, one enriched with P-TFA or one enriched with R-TFA. Diets were fed during either pregnancy alone or pregnancy and lactation. Weaned offspring were then transferred to an atherogenic diet for twelve weeks. Atherosclerosis was assessed as lipid staining in cross-sections of the aorta. Compared to those born of chow-fed dams, mice from those fed R-TFA or P-TFA during pregnancy alone were protected from aortic atherosclerosis (p=0.011 and 0.017, respectively). This was not associated with changes in total or lipoprotein cholesterol. Continuing to feed TFA during lactation increased atherosclerosis compared to that seen in offspring of dams fed TFA only during pregnancy (p= 0.024 and 0.028 for an interaction between diet and section number for P-TFA and R-TFA, respectively). We conclude that dietary TFA have differing effects on cardiovascular risk at different stages of the lifecycle.