UBC Theses and Dissertations
UBC Theses and Dissertations
Maternal diet fat alters milk fatty acids, suckling pups’ intestinal phospholipid fatty acids and intestinal responsiveness to experimental colitis Mundra, Harmeet Kaur
The quantity and quality of dietary lipids is crucial for infant growth and development. The significance of the differences in n-6 and n-3 fatty acids in human milk, and the effect of maternal diet fat on various inflammatory mediators in the gastrointestinal tract of infants have received little attention. The aims of the present study were to determine the effect of maternal dietary fat composition on rat milk, intestinal phospholipid fatty acids and responsiveness to experimental colitis in suckling rat pups. Female rats were fed isocaloric diets varying only in fat composition throughout gestation and lactation. The oils used were high in n-3 (canola oil, 8% 18:3n-3), n-6 (safflower oil, 72% 18:2n-6), or n-9 (high oleic acid safflower oil, 78% 18:ln-9) fatty acids, n=6 dams/ group. A reference group of rats fed chow (37% 18:2n-6, 4% 18:3n-3, l%20:5n-3, 2% 22:6n-3) were also studied. Colitis was induced in the pups on postnatal day 15 by intra-rectal dinitrobenzene sulfonic acid (DNBS) administration, with vehicle (50% ethanol) and procedure (0.9% saline) control pups. Jejunal and colonic phospholipids (phosphatidylcholine and phosphatidylethanolamine) and milk fatty acids were determined. The distal colon was assessed for macroscopic damage, histology and myeloperoxidase activity (MPO). The high n-6 maternal diet increased n-6 fatty acids, whereas the high n-3 diet increased n-3 fatty acids in milk and pup jejunal and colonic phospholipids. Maternal diet, milk and pup intestinal n-6/n-3 fatty acid ratios increased significantly in order: high 18:3n-3 < high 18:ln-9 < high 18:2n-6. DNBS administration in pups in the high 18:2n-6 group led to severe colitis with higher colonic damage scores and MPO activity than in 18:ln-9 and 18:3n-3 groups. High maternal dietary 18:3n-3 intake was associated with colonic damage scores and MPO activity that were not significantly different from ethanol controls. The composition of rat milk, pups intestinal fatty acids and n-6/n-3 fatty acid ratios in reference group were similar to high 18:3n-3 group, however, DNBS colitis was associated with higher colonic damage scores and MPO activity compared to high 18:3n-3 group. To conclude the maternal dietary fat influences the composition of rat milk fatty acids, intestinal lipids and responsiveness to experimental colitis in nursing offspring. Higher dietary n-3 fatty acids attenuate intestinal responsiveness to colitis. To the best of our knowledge, this is the first report to suggest that the composition of milk fatty acids is associated with the nursing offspring's susceptibility to chemically-induced colitis.
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