Intestinal responsiveness to experimental colitis in young rats is altered by maternal diet

Jacobson, Kevan; Mundra, Harmeet; Innis, Sheila M.

doi:10.1152/ajpgi.00459.2004

Cited by 32 publications

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“…The present study confirms and extends previous reports (24) to show that maternal diet n-6 and n-3 polyunsaturated fatty acids alter n-6 and n-3 fatty acids in rat milk, as is also known to occur in humans (20). More importantly, the maternal diet fatty acids had a marked effect on n-6 and n-3 fatty acids in the nursing infant's intestinal membranes.…”

Section: Discussionsupporting

confidence: 92%

“…However, placental transfer and secretion of n-6 and n-3 fatty acids in breast milk is variable and depends on the n-6 and n-3 fatty acids in the mother's diet, which in turn influences intestinal membrane fatty acid composition and mucosal response (20,21,24). In a previous study, we showed that 15-day-old neonates in the high n-6 linoleic acid (18:2n-6) dietary group had higher colonic membrane 20:4n-6 and a more severe inflammatory response to dinitrobenzene sulfonic acid (DNBS)-induced colitis than rats in the high 18:3n-3 dietary group associated with higher colonic membrane 20:5n-3 and docosahexaenoic acid (22:6n-3).…”

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confidence: 99%

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Perinatal lipid nutrition alters early intestinal development and programs the response to experimental colitis in young adult rats

Innis

Dai

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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The long-chain polyunsaturated n-6 and n-3 fatty acids are essential nutrients in membrane biogenesis and regulate gene expression via their eicosanoid metabolites. We investigated whether the n-6 and n-3 fatty acid supply as determined by maternal diet alters colonic phospholipid fatty acids, intestinal morphology, and epithelial barrier permeability during milk feeding with lasting effect on mucosal responsiveness to dinitrobenzene sulfonic acid (DNBS)-induced colitis in young adulthood. Female rats were fed diets with 20% energy from safflower oil (SO) or canola oil (CO), or 8% fish oil (FO) plus 2% SO (10% FO) or 18% FO plus 2% SO (20% FO) throughout gestation and lactation and offspring weaned to a standard diet at 21 days of age. At 15 days of age, pups in the 20% and 10% FO groups had lower 20:4n-6 and higher 20:5n-3 and 22:6n-3 in colon phospholipids (P Ͻ 0.01), shorter crypts (P Ͻ 0.05), and higher paracellular permeability than SO or CO groups. At 3 mo of age, male offspring in the FO groups showed lasting reduction of crypt depth and a heightened inflammatory response to DNBS. We demonstrate that early decreased colon 20: 4n-6 with increased n-3 fatty acids impairs intestinal barrier development and sensitizes the colon response to inflammatory insults later in life.n-6 fatty acids; n-3 fatty acids; arachidonic acid; milk fatty acids; intestinal programming; inflammatory bowel disease INFLAMMATORY BOWEL DISEASE (IBD), including Crohn disease and ulcerative colitis, are chronic recurrent inflammatory disorders thought to be precipitated by interplay of environmental and host immune factors in genetically susceptible individuals (40). A pivotal role of environmental factors is clear from the increasing incidence of IBD in recent decades in Western countries (4, 23, 34) and among migrant populations (37,38,43) and the emergence of IBD in populations with previously low prevalence (28).

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confidence: 92%

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confidence: 99%

Perinatal lipid nutrition alters early intestinal development and programs the response to experimental colitis in young adult rats

Innis

Dai

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…High intake of n-3 fatty acids is associated with a decrease in production of proinflammatory eicosanoids, cytokines, chemokines, reactive oxygen species and expression of adhesion molecules. In this study, rats were fed ad libitum diets identical in all nutrients except fatty acids, with as a percent energy from fat, 20% SO, 20% CO, or 18% fish oil plus 2% safflower oil (FO) [10][11] . As a percentage of the daily energy, the SO diet provided 15% linoleic acid (LA), with <0.06% α-linolenic acid (ALA) and no eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), the CO diet had 4.2% LA and 1.9% ALA with no EPA or DHA, and the FO diet provided 1.4% EPA, 4.9% DHA, 0.32% LA, and 0.12% ALA. Three weeks after initiation of the lipid diets, the mice were administered intrarectal DNBS or 50% ethanol and sacrificed 5 days later.…”

Section: Transmural Inflammationmentioning

confidence: 99%

“…Appropriate fixation of samples is a key to study both the histopathological damage and visualization of target molecules in tissues by H&E and immunostaining, respectively. Histological scoring of tissues should be performed by experienced individuals who are blinded to the experimental conditions, using fixed criteria set by the individual investigator 11,17 . Myeloperoxidase (MPO) serves as a good marker of inflammation, tissue injury and neutrophil infiltration into gastrointestinal tissues 11 .…”

Section: Collecting Tissues and Assessing Histological Damage In Dnbsmentioning

confidence: 99%

“…Histological scoring of tissues should be performed by experienced individuals who are blinded to the experimental conditions, using fixed criteria set by the individual investigator 11,17 . Myeloperoxidase (MPO) serves as a good marker of inflammation, tissue injury and neutrophil infiltration into gastrointestinal tissues 11 . To perform the MPO assays, it is suggested to snap freeze the tissues in liquid nitrogen and on the day of analysis, it is recommended to work with freshly prepared buffers and solutions to obtain the best and most accurate results.…”

Section: Collecting Tissues and Assessing Histological Damage In Dnbsmentioning

confidence: 99%

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DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Morampudi

Bhinder

et al. 2014

JoVE

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Inflammatory Bowel Diseases (IBD), including Crohn's Disease and Ulcerative Colitis, have long been associated with a genetic basis, and more recently host immune responses to microbial and environmental agents. Dinitrobenzene sulfonic acid (DNBS)-induced colitis allows one to study the pathogenesis of IBD associated environmental triggers such as stress and diet, the effects of potential therapies, and the mechanisms underlying intestinal inflammation and mucosal injury. In this paper, we investigated the effects of dietary n-3 and n-6 fatty acids on the colonic mucosal inflammatory response to DNBS-induced colitis in rats. All rats were fed identical diets with the exception of different types of fatty acids [safflower oil (SO), canola oil (CO), or fish oil (FO)] for three weeks prior to exposure to intrarectal DNBS. Control rats given intrarectal ethanol continued gaining weight over the 5 day study, whereas, DNBS-treated rats fed lipid diets all lost weight with FO and CO fed rats demonstrating significant weight loss by 48 hr and rats fed SO by 72 hr. Weight gain resumed after 72 hr post DNBS, and by 5 days post DNBS, the FO group had a higher body weight than SO or CO groups. Colonic sections collected 5 days post DNBS-treatment showed focal ulceration, crypt destruction, goblet cell depletion, and mucosal infiltration of both acute and chronic inflammatory cells that differed in severity among diet groups. The SO fed group showed the most severe damage followed by the CO, and FO fed groups that showed the mildest degree of tissue injury. Similarly, colonic myeloperoxidase (MPO) activity, a marker of neutrophil activity was significantly higher in SO followed by CO fed rats, with FO fed rats having significantly lower MPO activity. These results demonstrate the use of DNBS-induced colitis, as outlined in this protocol, to determine the impact of diet in the pathogenesis of IBD. Video LinkThe video component of this article can be found at

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Maternal high‐fat diet consumption enhances offspring susceptibility to DSS‐induced colitis in mice

Bibi

Kang

et al. 2017

Obesity

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Intestinal responsiveness to experimental colitis in young rats is altered by maternal diet

Abstract: Jacobson, Kevan, Harmeet Mundra, and Sheila M. Innis. Intestinal responsiveness to experimental colitis in young rats is altered by maternal diet.

Cited by 32 publications

References 50 publications

Perinatal lipid nutrition alters early intestinal development and programs the response to experimental colitis in young adult rats

Perinatal lipid nutrition alters early intestinal development and programs the response to experimental colitis in young adult rats

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Maternal high‐fat diet consumption enhances offspring susceptibility to DSS‐induced colitis in mice

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