Our research: Maternal trans-fats and programming of cardiovascular disease.


Trans-fatty acids are unsaturated fatty acids in which double bonds exist in the trans-isomer configuration. This is rare in nature as most fatty acids produced through biological processes have cis-double bonds. Trans-fatty acids in the food chain are therefore mostly generated through industrial processing in which hydrogenation of oils to produce solid fats changes the chemical structure of the fatty acids. Industrially generated trans-fatty acids are known to be associated with cardiovascular disease as they increase concentrations of low density lipoprotein cholesterol. In the US levels of trans-fatty acids in food are considered unsafe and a ban is likely to emerge in the near future. Other countries have legal limits on industrial trans-fatty acids in food. Trans fatty acids are also present in produce from ruminants as these animals produce vaccenic acid and conjugated linoleic acid in milk and meat. There is some evidence that ruminant-derived fatty acids may be beneficial to cardiovascular health.

Our group is interested in the early life origins of disease and it was therefore of interest to evaluate whether early life exposure to trans-fatty acids might impact upon risk of atherosclerosis in adult life. Our project, funded by the US Department of Agriculture (PI Adam Lock, CoIs Andy Salter, Simon Langley-Evans) utilised the ApoE*3 Leiden mouse to evaluate the effects of feeding different sources of trans-fatty acids during pregnancy alone, or during pregnancy and lactation upon the development of atherosclerosis in the offspring. The ApoE*3 Leiden mouse is a transgenic mouse which carries a mutated human ApoE3 gene. This mutation means that the mice will develop atherosclerosis when fed a high cholesterol, atherogenic diet. There is generally a relationship between the intake of cholesterol and the extent of atherosclerosis, but we have previously shown that variation in the maternal diet can impact upon the extent of atherosclerosis developed in response to atherogenic diet.

In the USDA funded study, offspring carrying the ApoE*3 Leiden gene were generated by mating wild type female mice with transgenic males. The pregnant mice were then fed diets either containing industrial trans-fats or ruminant-derived trans-fats during pregnancy. Offspring with the ApoE*3 Leiden gene were then selected for feeding either standard mouse diet or atherogenic diet. Atherosclerotic plaque formation was measured in these adult offspring. We hope to publish the findings from this work shortly.

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