Document Detail

An enteral formula containing fish oil, indigestible oligosaccharides, gum arabic and antioxidants affects plasma and colonic phospholipid fatty acid and prostaglandin profiles in pigs.
MedLine Citation:
PMID:  9040557     Owner:  NLM     Status:  MEDLINE    
Evidence supports a pathogenic role of arachidonic acid-derived inflammatory mediators within the gastrointestinal tract of patients with inflammatory bowel disease. The purpose of this study was to assess the effects of an ulcerative colitis nutritional formula (UCNF) containing oligosaccharides, fish oil, gum arabic and antioxidants on plasma and colonic phospholipid fatty acid and prostaglandin profiles in pigs. Twenty-four growing barrows in two replications were equally randomized among four killing times (d 0, 7, 14 and 21), and one of two diets, a control and the UCNF. Diets contained comparable levels of protein, fat, and nonstructural carbohydrate and met 100% of the energy requirements of the pig. Intake and body weight were recorded daily while blood, urine and tissue samples were collected at time of kill. Within 1 wk of ingestion of the UCNF, the composition of plasma phospholipid fatty acids showed an increase in 20:5(n-3) and 22:6(n-3) (P < 0.0001) and a decrease in 20:4(n-6) and 18:2(n-6) (P < 0.0001). Similar effects were observed for the phospholipids in the colonic and cecal mucosa. Plasma prostaglandin E was unaffected by treatment, whereas thromboxane B2 and 6-keto-prostaglandin F1 alpha levels were significantly decreased after 7 d of UCNF ingestion. Ingestion of the UCNF resulted in a suppression in the synthesis of proinflammatory prostaglandins by cecal and colonic mucosal cells. Levels of colonic and cecal prostaglandin E, 6-keto-prostaglandin F1 alpha and thromboxane B2 were significantly decreased after 7 d of UCNF ingestion. These changes may have been mediated by rapid increases of (n-3) fatty acids into cellular phospholipids. Dietary supplementation with the UCNF may prove beneficial for patients with ulcerative colitis by modulating colonic prostaglandin synthesis.
J M Campbell; G C Fahey; C A Lichtensteiger; S J Demichele; K A Garleb
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Journal of nutrition     Volume:  127     ISSN:  0022-3166     ISO Abbreviation:  J. Nutr.     Publication Date:  1997 Jan 
Date Detail:
Created Date:  1997-03-19     Completed Date:  1997-03-19     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0404243     Medline TA:  J Nutr     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  137-45     Citation Subset:  IM    
Department of Animal Sciences, University of Illinois, Urbana 61801, USA.
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MeSH Terms
Animal Nutritional Physiological Phenomena
Antioxidants / administration & dosage*,  metabolism
Cecum / drug effects*,  metabolism*
Colon / drug effects*,  metabolism*
Enteral Nutrition
Excipients / administration & dosage*,  metabolism
Fish Oils / administration & dosage*,  metabolism
Gum Arabic / administration & dosage*,  metabolism
Oligosaccharides / administration & dosage*,  metabolism
Phospholipids / blood*,  metabolism
Prostaglandins / biosynthesis*,  blood
Reg. No./Substance:
0/Antioxidants; 0/Excipients; 0/Fish Oils; 0/Oligosaccharides; 0/Phospholipids; 0/Prostaglandins; 9000-01-5/Gum Arabic

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