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Nutritional Neuroscience
An International Journal on Nutrition, Diet and Nervous System
Volume 22, 2019 - Issue 4
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Articles

Maternal dietary n-6 polyunsaturated fatty acid deprivation does not exacerbate post-weaning reductions in arachidonic acid and its mediators in the mouse hippocampus

, , , &
Pages 223-234 | Published online: 13 Sep 2017
 

Abstract

Objectives: The present study examines how lowering maternal dietary n-6 polyunsaturated fatty acids (PUFA) (starting from pregnancy) compared to offspring (starting from post-weaning) affect the levels of n-6 and n-3 fatty acids in phospholipids (PL) and lipid mediators in the hippocampus of mice.

Methods: Pregnant mice were randomly assigned to consume either a deprived or an adequate n-6 PUFA diet during pregnancy and lactation (maternal exposure). On postnatal day (PND) 21, half of the male pups were weaned onto the same diet as their dams, and the other half were switched to the other diet for 9 weeks (offspring exposure). At PND 84, upon head-focused high-energy microwave irradiation, hippocampi were collected for PL fatty acid and lipid mediator analyses.

Results: Arachidonic acid (ARA) concentrations were significantly decreased in both total PL and PL fractions, while eicosapentaenoic acid (EPA) concentrations were increased only in PL fractions upon n-6 PUFA deprivation of offspring, regardless of maternal exposure. Several ARA-derived eicosanoids were reduced, while some of the EPA-derived eicosanoids were elevated by n-6 PUFA deprivation in offspring. There was no effect of diet on docosahexaenoic acid (DHA) or DHA-derived docosanoids concentrations under either maternal or offspring exposure.

Discussion: These results indicate that the maternal exposure to dietary n-6 PUFA may not be as important as the offspring exposure in regulating hippocampal ARA and some lipid mediators. Results from this study will be helpful in the design of experiments aimed at testing the significance of altering brain ARA levels over different stages of life.

Acknowledgements

The authors thank Dr Denis Reynaud and Michael Leadley of the Analytical Facility for Bioactive Molecules at The Centre for the Study of Complex Childhood Diseases, The Hospital for Sick Children, Toronto, Canada for assistance with the LC-MS–MS. Travel support from Mead Johnson and mass spectrometry equipment and support from Sciex. RPB is on the executive of the International Society for the Study of Fatty acids and Lipids and held a meeting on behalf of Fatty Acids and Cell Signaling, both of which rely on corporate sponsorship. RPB has given expert testimony in relation to supplements and the brain. RPB also provides complementary fatty acid analysis for farmers, food producers and others involved in the food industry, some of whom provide free food samples.

Additional information

Funding

The work was supported by grant from the Canadian Institutes of Health Research to R.P.B under grant number (489524). S.M.A. received a studentship from King Abdul Aziz University in Jeddah, Saudi Arabia under grant number (20977) and R.P.B. holds a Canada Research Chair in Brain Lipid Metabolism. R.P.B. has received research grants from Bunge Ltd, Arctic Nutrition, the Dairy Farmers of Canada and Nestle Inc.

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