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DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
Published on: February 27, 2014
Intestinal responsiveness to experimental colitis in young rats is altered by maternal diet
Kevan Jacobson1, Harmeet Mundra, Sheila M Innis
1Division of Gastroenterology, Department of Pediatrics and Nutrition Research Program, British Columbia Institute for Children's and Women's Health, University of British Columbia, Vancouver, British Columbia, Canada. kjacobson@cw.bc.ca
Insights
Maternal diet fat composition significantly alters offspring
Area of Science:
- Nutritional science and developmental biology.
- Gastroenterology and immunology.
- Perinatal nutrition and long-term health outcomes.
Background:
- Fetal and neonatal nutrition are critical determinants of later-life health.
- Maternal dietary fat intake can influence offspring's physiological development.
- The impact of specific maternal fatty acid profiles on infant gut health and disease susceptibility is not fully understood.
Purpose of the Study:
- To investigate how maternal dietary fat composition affects intestinal phospholipid fatty acids in suckling rat pups.
- To determine the influence of maternal diet on the susceptibility of offspring to experimental colitis.
- To establish the relationship between maternal fatty acid intake, milk composition, and offspring's gut inflammatory response.
Main Methods:
- Female rats were fed diets high in n-3, n-6, or n-9 fatty acids during gestation and lactation.
- Colitis was induced in pups using 2,4-dinitrobenzene sulfonic acid (DNBS) on postnatal day 15.
- Analysis included jejunal and colonic phospholipids, milk fatty acids, colonic damage scores, and myeloperoxidase (MPO) activity.
Main Results:
- Maternal diets rich in n-3 or n-6 fatty acids altered milk and pup intestinal phospholipid fatty acid profiles accordingly.
- The n-6 to n-3 fatty acid ratio in maternal diet, milk, and pup intestines increased in the order: n-3 < n-9 < n-6.
- Pups from mothers fed a high n-6 diet exhibited more severe colitis, with higher damage scores and MPO activity, compared to other groups.
Conclusions:
- Maternal dietary fat composition directly influences the fatty acid composition of intestinal lipids in nursing offspring.
- A high maternal n-6 fatty acid intake exacerbates experimental colitis in rat pups.
- Maternal intake of n-3 fatty acids (canola oil) conferred protection against DNBS-induced colitis in offspring.
Abstract:
Increasing evidence suggests that fetal and neonatal nutrition impacts later health. Aims of the present study were to determine the effect of maternal dietary fat composition on 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 (8%) in n-3 [canola oil (18:3n-3)], n-6 (72%) [safflower oil (18:2n-6)], or n-9 (78%) [high oleic acid safflower oil (18:1n-9)] fatty acids, n = 6/group. Colitis was induced on postnatal day 15 by intrarectal 2,4-dinitrobenzene sulfonic acid (DNBS) administration with vehicle (50% ethanol) and procedure (0.9% saline) controls. Jejunal and colonic phospholipids and milk fatty acids were determined. The distal colon was assessed for macroscopic damage, histology, and MPO activity. The 18:2n-6 maternal diet increased n-6 fatty acids, whereas the 18:3n-3 diet increased n-3 fatty acids in milk and pup jejunal and colonic phospholipids. Maternal diet, milk, and pup intestinal n-6-to-n-3 fatty acid ratios increased significantly in order: high 18:3n-3 < high 18:1n-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 the 18:1n-9 and 18:3n-3 groups. High maternal dietary 18:3n-3 intake was associated with colonic damage scores and MPO activity, which were not significantly different from ethanol controls. We demonstrate that maternal dietary fat influences the composition of intestinal lipids and responsiveness to experimental colitis in nursing offspring.

