Nutritional Regulation: Inflammatory bowel disease is an umbrella term used to describe a group of gastrointestinal diseases characterized by chronic, ongoing inflammation of all or part of the gastrointestinal tract, or GI tract, such as Crohn’s disease, or CD, and ulcerative colitis, UC. While many factors have been determined to cause inflammatory bowel disease, research studies have concluded that nutrition can increase the risk of gastrointestinal diseases, including inflammatory bowel disease.
How does nutrition affect inflammatory bowel disease?
Nutrient deficiencies are common among individuals with inflammatory bowel disease, or IBD. Both complete parenteral and enteral nutrition can provide significant supportive treatment for patients with IBD, however, in adults those alone may not be helpful as a form of primary treatment. Clinical intervention using omega-3 polyunsaturated fatty acids found in fish oil could be beneficial for the nutritional regulation of IBD patients and recent research studies have emphasized the function of PPAR on NF?B action towards its possible beneficial impact on dietary lipids for overall intestinal functioning.
Nutrition in Inflammatory Bowel Disease
Specific antibody isotypes of essential milk proteins are located in both UC and CD patients. In CD, the antibodies are associated with disease. Although cultural origin, rather than the IBD disease condition, seems to be the primary cause of lactose intolerance, the avoidance of milk products by IBD patients is extensive. Lack of breast-feeding during infancy was associated with CD but not UC. Additionally, higher carbohydrate intake was recorded in CD. Others have suggested a deficiency of dietary fiber as a predisposing factor for IBD. The growth of UC has also been associated with higher intakes of polyunsaturated fatty acids (MUFA), n6 polyunsaturated fatty acids (n6 PUFA), sulphur-containing diets and vitamin B6.
Deficiencies: Nutritional Regulation
Inflammatory bowel disease is related to several nutritional deficiencies, such as anemia, hypoalbuminemia, hypomagnesia, hypocalcemia and hypophosphatemia, including deficiencies in folic acid, niacin, vitamins A, B12, C, and D, in addition to deficiencies of iron, magnesium and zinc. Further research studies are needed to determine if reduced levels of micronutrients are of some significance to the result of gastrointestinal diseases. Plasma antioxidant concentrations are lower in IBD patients, especially those who have an active form of the disease. Antioxidant action, evaluated by measuring selenium levels and erythrocyte glutathione peroxidase activity, is inversely associated with inflammatory biomarkers, such as TNF?. Hyperhomocysteinemia is more prevalent in patients with IBD, and is characterized with low serum as well as reduced concentrations of vitamin B12, folate and B6.
Several mechanisms are responsible for the malnutrition observed in IBD patients. Primarily, there’s a decline in the oral consumption of nutrients due to abdominal pain and anorexia. Second, the mucosal inflammation and related diarrhea reduces blood, protein, minerals, electrolytes and trace components. Paradoxically, multiple resections or bacterial vaginosis might have an adverse nutrient impact; and finally, herbal remedies may also cause malnutrition. By way of instance, sulfasalazine reduces nitric acid absorption, and corticosteroids reduce calcium absorption in addition to negatively impacting protein metabolism. Alterations in energy metabolism may result in increased resting energy expenditure and lipid oxidation in patients with inflammatory bowel disease. There are many effects of malnutrition and each can decrease bone mineral density, in addition to growth retardation and delayed sexual maturity in children. Osteoporosis may also be involved as a consequence of pro-inflammatory cytokine profiles.
Nutritional treatment may take on a range of forms including Total Parenteral Nutrition (TPN) and Complete Enteral Nutrition (TEN). The diets used are elemental, polymeric, and exception diets. Elemental diets contain nutrients reduced to their fundamental elements: amino acids, such as proteins, sugar for carbs, and short-chain triglycerides, such as fats. Polymeric formulas contain entire proteins, such as nitrogen, glucose polymers for carbs and long-chain triglycerides for fat or starch.
Total Parenteral Nutrition (TPN)
Using TPN for the nutritional regulation of IBD is based on specific theoretical benefits, including how: gut rest may be beneficial since it reduces motor and transportation function in the diseased intestine; a drop in antigenic stimulation can remove the immunologic reactions to food, particularly in the presence of diminished intestinal permeability; TPN promotes protein synthesis in the gut which provides cell renewal, recovery, and alteration of impaired immunocompetence.
Researchers demonstrated remission rates of 63 percent to 89 percent with TPN in a large retrospective collection of CD patients which were difficult in standard medical management. But, Matuchansky et al highlighted that there have been high relapse rates (40%-62%) after two decades. It’s been implied that TPN be utilized exclusively in a nutritionally supportive function. In UC, there’s absolutely no evidence for much better results with TPN. Though remission rates of 9 percent to 80 percent are reported, TPN provided to patients with acute colitis seems to be beneficial as perioperative nutritional support. In patients with moderate disease, TPN is significantly more successful but isn’t better than steroid treatment, and so the invasiveness and price of TPN are unjustified. Any advantages related to TPN might be due to the nutritional regulation, rather than gut rest, as gut rest alone has no impact on disease activity. Accordingly, though TPN has a function in patients using a non-functioning gut or the brief gut syndrome because of excess resections, TPN is of limited use as a primary treatment in IBD. This isn’t designed to be an extensive breakdown of TPN, but it needs to be cautioned that in specialist centers, TPN is associated with complications like sepsis and cholestatic liver disease.
Total enteral nutrition (TEN), Elemental & Defined Formula Diets
TEN prevents possible toxic dietary variables and antigenic exposure, because there are only amino acids, sugar or oligosaccharides and very low lipid content. TEN isn’t associated with cholestasis, biliary sludge or gallstone formation, as can be observed with TPN. Atrophy of the small intestinal mucosa was discovered in animal models receiving long-term TPN, yet this atrophy is prevented with TEN. Additionally, a 6-wk TPN therapy in dogs led to marked decrease in pancreatic fat, a reduction in small intestinal mass as well as a decline in intestinal disaccharidase activity in puppies. Because of this, TEN is more preferable than TPN.
The subject of nutrition in gastrointestinal disorders which occur in IBD has been recently reviewd. In comparison to TPN, enteral nutrition yielded similar outcomes towards preventing and combating malnutrition. Though Voitk et al suggested that elemental diets could be an effective treatment for IBD, enteral nutrition as a primary therapy has failed to produce consistent results in several clinical trials. It’s correct that quite a few trials have shown remission levels in CD patients getting elemental diets, like the rates observed with prostate cancer treatment. But, it’s important to note that greater remission rates were detected in patients receiving steroid therapy versus standard diets when including all of the diet category fall outs (i.e., in an intent-to-treat foundation). The question remains concerning the best means of assessing the results when a sizable proportion of individuals receiving diet treatment fall out due to unpalatibility or intolerance. What’s more, a few research studies have demonstrated no distinction with elemental diets compared to steroid treatment. In children, elemental diets have been associated with higher linear gain, whereas in adults those diets maintain nitrogen equilibrium. The use of supplements in the context of pediatric onset illness was also reviewed. Therefore, enteral nutrition is simpler to use, is less costly, and it’s also a far better choice than TPN. Unfortunately, its unpalatability limits individual agreement, but with powerful encouragement this might be partly overcome.
The fat composition of enteral diets can influence the results that are obtained in the several clinical trials. Elemental diets include a reduced fat content, although a lot of healthier diets generally contain more fat, such as more lactic acid, which can be a precursor for the synthesis of possible pro-inflammatory eicosanoids.
Defined formula diets are often more palatable and more affordable than would be the elemental diets. When some researchers reported no gaps between utopian and defined formula diets in patients with severe CD, Giaffer et al discovered elemental diets are far more successful for active CD. A randomized double-blind study in Crohn’s patients revealed that elemental and polymeric, or characterized, diets differing only in their own source of nitrogen, were equally effective in lessening the Crohn’s disease activity index, or CDAI, also inducing clinical remission. Though defined formula diets supply less gut rest, they have the possible benefit of exposing the GI tract to the typical dietary substrates, which permit thereby for the complete manifestation of intestinal, biliary and pancreatic action. In animal research, it has also been discovered that luminal nutrition has trophic impacts on the intestine.
Can there be a beneficial effect of supplementing polymeric formulas with TGF-?1? In pediatric CD, reductions in pro-inflammatory cytokine concentrations and mRNA, paired with an up-regulation of TGF-? mRNA, was associated with enhanced macroscopic and microscopic mucosal inflammation. A meta-analysis along with a Cochrane review have demonstrated that in adults, corticosteroids are more effective than enteral diet treatment. It’s uncertain what is the use of supplements in adults with CD, even though there are some signs in Japan that enteral nutrition enjoys support as principal treatment. In contrast to this generally agreed part in adults of enteral nutrition being used to enhance the patient’s nutritional status because its principal advantage, in children with CD enteral nutrition has a far clearer benefit to enhance clinical, biochemical and growth parameters, and may as well have a steroid sparing effect.
Information referenced from the National Center for Biotechnology Information (NCBI) and the National University of Health Sciences. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
1. Liu Y, van Kruiningen HJ, West AB, Cartun RW, Cortot A, Colombel JF. Immunocytochemical evidence of Listeria, Escherichia coli, and Streptococcus antigens in Crohn’s disease. Gastroenterology. 1995;108:1396–1404. [PubMed]
2. Sartor R. Microbial factors in the pathogenesis of Crohn’s disease, ulcerative colitis and experimental intestinal inflammation. Baltimore: Williams & Wilkins; 1995.
3. Wakefield AJ, Ekbom A, Dhillon AP, Pittilo RM, Pounder RE. Crohn’s disease: pathogenesis and persistent measles virus infection. Gastroenterology. 1995;108:911–916. [PubMed]
4. Sartor RB. Current concepts of the etiology and pathogenesis of ulcerative colitis and Crohn’s disease. Gastroenterol Clin North Am. 1995;24:475–507. [PubMed]
5. Sartor RB. Pathogenesis and immune mechanisms of chronic inflammatory bowel diseases. Am J Gastroenterol. 1997;92:5S–11S. [PubMed]
6. MacDermott RP. Alterations in the mucosal immune system in ulcerative colitis and Crohn’s disease. Med Clin North Am. 1994;78:1207–1231. [PubMed]
7. Podolsky DK. Inflammatory bowel disease (1) N Engl J Med. 1991;325:928–937. [PubMed]
8. Podolsky DK. Inflammatory bowel disease (2) N Engl J Med. 1991;325:1008–1016. [PubMed]
9. Yang H, Rotter J. The genetics of inflammatory disease. Baltimore: Williams & Wilkins; 1994.
10. Wurzelmann JI, Lyles CM, Sandler RS. Childhood infections and the risk of inflammatory bowel disease. Dig Dis Sci. 1994;39:555–560. [PubMed]
11. Knoflach P, Park BH, Cunningham R, Weiser MM, Albini B. Serum antibodies to cow’s milk proteins in ulcerative colitis and Crohn’s disease. Gastroenterology. 1987;92:479–485. [PubMed]
12. De Palma GD, Catanzano C. Removable self-expanding metal stents: a pilot study for treatment of achalasia of the esophagus. Endoscopy. 1998;30:S95–S96. [PubMed]
13. Bernstein CN, Ament M, Artinian L, Ridgeway J, Shanahan F. Milk tolerance in adults with ulcerative colitis. Am J Gastroenterol. 1994;89:872–877. [PubMed]
14. Matsui T, Iida M, Fujishima M, Imai K, Yao T. Increased sugar consumption in Japanese patients with Crohn’s disease. Gastroenterol Jpn. 1990;25:271. [PubMed]
15. Kelly DG, Fleming CR. Nutritional considerations in inflammatory bowel diseases. Gastroenterol Clin North Am. 1995;24:597–611. [PubMed]
16. Geerling BJ, Dagnelie PC, Badart-Smook A, Russel MG, Stockbrügger RW, Brummer RJ. Diet as a risk factor for the development of ulcerative colitis. Am J Gastroenterol. 2000;95:1008–1013. [PubMed]
17. Dudrick SJ, Latifi R, Schrager R. Nutritional management of inflammatory bowel disease. Surg Clin North Am. 1991;71:609–623. [PubMed]
18. D’Odorico A, Bortolan S, Cardin R, D’Inca’ R, Martines D, Ferronato A, Sturniolo GC. Reduced plasma antioxidant concentrations and increased oxidative DNA damage in inflammatory bowel disease. Scand J Gastroenterol. 2001;36:1289–1294. [PubMed]
19. Reimund JM, Hirth C, Koehl C, Baumann R, Duclos B. Antioxidant and immune status in active Crohn’s disease. A possible relationship. Clin Nutr. 2000;19:43–48. [PubMed]
20. Romagnuolo J, Fedorak RN, Dias VC, Bamforth F, Teltscher M. Hyperhomocysteinemia and inflammatory bowel disease: prevalence and predictors in a cross-sectional study. Am J Gastroenterol. 2001;96:2143–2149. [PubMed]
21. Lewis JD, Fisher RL. Nutrition support in inflammatory bowel disease. Med Clin North Am. 1994;78:1443–1456. [PubMed]
22. Azcue M, Rashid M, Griffiths A, Pencharz PB. Energy expenditure and body composition in children with Crohn’s disease: effect of enteral nutrition and treatment with prednisolone. Gut. 1997;41:203–208.[PMC free article] [PubMed]
23. Mingrone G, Capristo E, Greco AV, Benedetti G, De Gaetano A, Tataranni PA, Gasbarrini G. Elevated diet-induced thermogenesis and lipid oxidation rate in Crohn disease. Am J Clin Nutr. 1999;69:325–330.[PubMed]
24. Bjarnason I, Macpherson A, Mackintosh C, Buxton-Thomas M, Forgacs I, Moniz C. Reduced bone density in patients with inflammatory bowel disease. Gut. 1997;40:228–233. [PMC free article] [PubMed]
25. Griffiths AM, Nguyen P, Smith C, MacMillan JH, Sherman PM. Growth and clinical course of children with Crohn’s disease. Gut. 1993;34:939–943. [PMC free article] [PubMed]
26. Fischer JE, Foster GS, Abel RM, Abbott WM, Ryan JA. Hyperalimentation as primary therapy for inflammatory bowel disease. Am J Surg. 1973;125:165–175. [PubMed]
27. Reilly J, Ryan JA, Strole W, Fischer JE. Hyperalimentation in inflammatory bowel disease. Am J Surg. 1976;131:192–200. [PubMed]
28. Ganem D, Schneider RJ. Hepadnaviridae: The viruses and their replication. In: Knipe DM, Howley PM, editors. Fields Virology. Volume 2. Philadelphia: Lippincott, Williams & Wilkins; 2001. pp. 2923–2969.
29. Jones VA, Dickinson RJ, Workman E, Wilson AJ, Freeman AH, Hunter JO. Crohn’s disease: maintenance of remission by diet. Lancet. 1985;2:177–180. [PubMed]
30. Suzuki I, Kiyono H, Kitamura K, Green DR, McGhee JR. Abrogation of oral tolerance by contrasuppressor T cells suggests the presence of regulatory T-cell networks in the mucosal immune system. Nature. 1986;320:451–454. [PubMed]
31. Ostro MJ, Greenberg GR, Jeejeebhoy KN. Total parenteral nutrition and complete bowel rest in the management of Crohn’s disease. JPEN J Parenter Enteral Nutr. 1985;9:280–287. [PubMed]
32. Matuchansky C. Parenteral nutrition in inflammatory bowel disease. Gut. 1986;27 Suppl 1:81–84.[PMC free article] [PubMed]
33. Payne-James JJ, Silk DB. Total parenteral nutrition as primary treatment in Crohn’s disease–RIP? Gut. 1988;29:1304–1308. [PMC free article] [PubMed]
34. Shiloni E, Coronado E, Freund HR. Role of total parenteral nutrition in the treatment of Crohn’s disease. Am J Surg. 1989;157:180–185. [PubMed]
35. Dickinson RJ, Ashton MG, Axon AT, Smith RC, Yeung CK, Hill GL. Controlled trial of intravenous hyperalimentation and total bowel rest as an adjunct to the routine therapy of acute colitis. Gastroenterology. 1980;79:1199–1204. [PubMed]
36. McIntyre PB, Powell-Tuck J, Wood SR, Lennard-Jones JE, Lerebours E, Hecketsweiler P, Galmiche JP, Colin R. Controlled trial of bowel rest in the treatment of severe acute colitis. Gut. 1986;27:481–485.[PMC free article] [PubMed]
37. Greenberg GR, Fleming CR, Jeejeebhoy KN, Rosenberg IH, Sales D, Tremaine WJ. Controlled trial of bowel rest and nutritional support in the management of Crohn’s disease. Gut. 1988;29:1309–1315.[PMC free article] [PubMed]
38. Hughes CA, Bates T, Dowling RH. Cholecystokinin and secretin prevent the intestinal mucosal hypoplasia of total parenteral nutrition in the dog. Gastroenterology. 1978;75:34–41. [PubMed]
39. Stratton RJ, Smith TR. Role of enteral and parenteral nutrition in the patient with gastrointestinal and liver disease. Best Pract Res Clin Gastroenterol. 2006;20:441–466. [PubMed]
40. O’Sullivan M, O’Morain C. Nutrition in inflammatory bowel disease. Best Pract Res Clin Gastroenterol. 2006;20:561–573. [PubMed]
41. González-Huix F, Fernández-Bañares F, Esteve-Comas M, Abad-Lacruz A, Cabré E, Acero D, Figa M, Guilera M, Humbert P, de León R. Enteral versus parenteral nutrition as adjunct therapy in acute ulcerative colitis. Am J Gastroenterol. 1993;88:227–232. [PubMed]
42. Voitk AJ, Echave V, Feller JH, Brown RA, Gurd FN. Experience with elemental diet in the treatment of inflammatory bowel disease. Is this primary therapy? Arch Surg. 1973;107:329–333. [PubMed]
43. Axelsson C, Jarnum S. Assessment of the therapeutic value of an elemental diet in chronic inflammatory bowel disease. Scand J Gastroenterol. 1977;12:89–95. [PubMed]
44. Lochs H, Steinhardt HJ, Klaus-Wentz B, Zeitz M, Vogelsang H, Sommer H, Fleig WE, Bauer P, Schirrmeister J, Malchow H. Comparison of enteral nutrition and drug treatment in active Crohn’s disease. Results of the European Cooperative Crohn’s Disease Study. IV. Gastroenterology. 1991;101:881–888.[PubMed]
45. Malchow H, Steinhardt HJ, Lorenz-Meyer H, Strohm WD, Rasmussen S, Sommer H, Jarnum S, Brandes JW, Leonhardt H, Ewe K. Feasibility and effectiveness of a defined-formula diet regimen in treating active Crohn’s disease. European Cooperative Crohn’s Disease Study III. Scand J Gastroenterol. 1990;25:235–244. [PubMed]
46. O’Brien CJ, Giaffer MH, Cann PA, Holdsworth CD. Elemental diet in steroid-dependent and steroid-refractory Crohn’s disease. Am J Gastroenterol. 1991;86:1614–1618. [PubMed]
47. Okada M, Yao T, Yamamoto T, Takenaka K, Imamura K, Maeda K, Fujita K. Controlled trial comparing an elemental diet with prednisolone in the treatment of active Crohn’s disease. Hepatogastroenterology. 1990;37:72–80. [PubMed]
48. O’Moráin C, Segal AW, Levi AJ. Elemental diet as primary treatment of acute Crohn’s disease: a controlled trial. Br Med J (Clin Res Ed) 1984;288:1859–1862. [PMC free article] [PubMed]
49. Raouf AH, Hildrey V, Daniel J, Walker RJ, Krasner N, Elias E, Rhodes JM. Enteral feeding as sole treatment for Crohn’s disease: controlled trial of whole protein v amino acid based feed and a case study of dietary challenge. Gut. 1991;32:702–707. [PMC free article] [PubMed]
50. Rocchio MA, Cha CJ, Haas KF, Randall HT. Use of chemically defined diets in the management of patients with acute inflammatory bowel disease. Am J Surg. 1974;127:469–475. [PubMed]
51. Saverymuttu S, Hodgson HJ, Chadwick VS. Controlled trial comparing prednisolone with an elemental diet plus non-absorbable antibiotics in active Crohn’s disease. Gut. 1985;26:994–998. [PMC free article][PubMed]
52. Teahon K, Bjarnason I, Pearson M, Levi AJ. Ten years’ experience with an elemental diet in the management of Crohn’s disease. Gut. 1990;31:1133–1137. [PMC free article] [PubMed]
53. Teahon K, Smethurst P, Pearson M, Levi AJ, Bjarnason I. The effect of elemental diet on intestinal permeability and inflammation in Crohn’s disease. Gastroenterology. 1991;101:84–89. [PubMed]
54. Heuschkel RB, Menache CC, Megerian JT, Baird AE. Enteral nutrition and corticosteroids in the treatment of acute Crohn’s disease in children. J Pediatr Gastroenterol Nutr. 2000;31:8–15. [PubMed]
55. Sanderson IR, Boulton P, Menzies I, Walker-Smith JA. Improvement of abnormal lactulose/rhamnose permeability in active Crohn’s disease of the small bowel by an elemental diet. Gut. 1987;28:1073–1076.[PMC free article] [PubMed]
56. Sanderson IR, Udeen S, Davies PS, Savage MO, Walker-Smith JA. Remission induced by an elemental diet in small bowel Crohn’s disease. Arch Dis Child. 1987;62:123–127. [PMC free article] [PubMed]
57. Ruemmele FM, Roy CC, Levy E, Seidman EG. Nutrition as primary therapy in pediatric Crohn’s disease: fact or fantasy? J Pediatr. 2000;136:285–291. [PubMed]
58. O’Morain C, O’Sullivan M. Nutritional support in Crohn’s disease: current status and future directions. J Gastroenterol. 1995;30 Suppl 8:102–107. [PubMed]
59. Rigaud D, Cosnes J, Le Quintrec Y, René E, Gendre JP, Mignon M. Controlled trial comparing two types of enteral nutrition in treatment of active Crohn’s disease: elemental versus polymeric diet. Gut. 1991;32:1492–1497. [PMC free article] [PubMed]
60. Royall D, Wolever TM, Jeejeebhoy KN. Evidence for colonic conservation of malabsorbed carbohydrate in short bowel syndrome. Am J Gastroenterol. 1992;87:751–756. [PubMed]
61. Giaffer MH, North G, Holdsworth CD. Controlled trial of polymeric versus elemental diet in treatment of active Crohn’s disease. Lancet. 1990;335:816–819. [PubMed]
62. Verma S, Kirkwood B, Brown S, Giaffer MH. Oral nutritional supplementation is effective in the maintenance of remission in Crohn’s disease. Dig Liver Dis. 2000;32:769–774. [PubMed]
63. Levine GM, Deren JJ, Steiger E, Zinno R. Role of oral intake in maintenance of gut mass and disaccharide activity. Gastroenterology. 1974;67:975–982. [PubMed]
64. Weser E, Heller R, Tawil T. Stimulation of mucosal growth in the rat ileum by bile and pancreatic secretions after jejunal resection. Gastroenterology. 1977;73:524–529. [PubMed]
65. Fell JM, Paintin M, Arnaud-Battandier F, Beattie RM, Hollis A, Kitching P, Donnet-Hughes A, MacDonald TT, Walker-Smith JA. Mucosal healing and a fall in mucosal pro-inflammatory cytokine mRNA induced by a specific oral polymeric diet in paediatric Crohn’s disease. Aliment Pharmacol Ther. 2000;14:281–289. [PubMed]
66. Souba WW, Smith RJ, Wilmore DW. Glutamine metabolism by the intestinal tract. JPEN J Parenter Enteral Nutr. 1985;9:608–617. [PubMed]
67. Windmueller HG, Spaeth AE. Uptake and metabolism of plasma glutamine by the small intestine. J Biol Chem. 1974;249:5070–5079. [PubMed]
68. Higashiguchi T, Hasselgren PO, Wagner K, Fischer JE. Effect of glutamine on protein synthesis in isolated intestinal epithelial cells. JPEN J Parenter Enteral Nutr. 1993;17:307–314. [PubMed]
69. Burke DJ, Alverdy JC, Aoys E, Moss GS. Glutamine-supplemented total parenteral nutrition improves gut immune function. Arch Surg. 1989;124:1396–1399. [PubMed]
70. Souba WW, Herskowitz K, Klimberg VS, Salloum RM, Plumley DA, Flynn TC, Copeland EM. The effects of sepsis and endotoxemia on gut glutamine metabolism. Ann Surg. 1990;211:543–549; discussion 543-551;. [PMC free article] [PubMed]
71. Den Hond E, Hiele M, Peeters M, Ghoos Y, Rutgeerts P. Effect of long-term oral glutamine supplements on small intestinal permeability in patients with Crohn’s disease. JPEN J Parenter Enteral Nutr. 1999;23:7–11. [PubMed]
72. Akobeng AK, Miller V, Stanton J, Elbadri AM, Thomas AG. Double-blind randomized controlled trial of glutamine-enriched polymeric diet in the treatment of active Crohn’s disease. J Pediatr Gastroenterol Nutr. 2000;30:78–84. [PubMed]
73. Jacobs LR, Lupton JR. Effect of dietary fibers on rat large bowel mucosal growth and cell proliferation. Am J Physiol. 1984;246:G378–G385. [PubMed]
74. Spaeth G, Berg RD, Specian RD, Deitch EA. Food without fiber promotes bacterial translocation from the gut. Surgery. 1990;108:240–246; discussion 246-247;. [PubMed]
75. Roediger WE, Moore A. Effect of short-chaim fatty acid on sodium absorption in isolated human colon perfused through the vascular bed. Dig Dis Sci. 1981;26:100–106. [PubMed]
76. Sakata T. Stimulatory effect of short-chain fatty acids on epithelial cell proliferation in the rat intestine: a possible explanation for trophic effects of fermentable fibre, gut microbes and luminal trophic factors. Br J Nutr. 1987;58:95–103. [PubMed]
77. Roediger WE. The colonic epithelium in ulcerative colitis: an energy-deficiency disease? Lancet. 1980;2:712–715. [PubMed]
78. Chapman MA, Grahn MF, Boyle MA, Hutton M, Rogers J, Williams NS. Butyrate oxidation is impaired in the colonic mucosa of sufferers of quiescent ulcerative colitis. Gut. 1994;35:73–76.[PMC free article] [PubMed]
79. Den Hond E, Hiele M, Evenepoel P, Peeters M, Ghoos Y, Rutgeerts P. In vivo butyrate metabolism and colonic permeability in extensive ulcerative colitis. Gastroenterology. 1998;115:584–590. [PubMed]
80. Simpson EJ, Chapman MA, Dawson J, Berry D, Macdonald IA, Cole A. In vivo measurement of colonic butyrate metabolism in patients with quiescent ulcerative colitis. Gut. 2000;46:73–77.[PMC free article] [PubMed]
81. Tappenden KA, Thomson AB, Wild GE, McBurney MI. Short-chain fatty acid-supplemented total parenteral nutrition enhances functional adaptation to intestinal resection in rats. Gastroenterology. 1997;112:792–802. [PubMed]
82. Senagore AJ, MacKeigan JM, Scheider M, Ebrom JS. Short-chain fatty acid enemas: a cost-effective alternative in the treatment of nonspecific proctosigmoiditis. Dis Colon Rectum. 1992;35:923–927.[PubMed]
83. Segain JP, Raingeard de la Blétière D, Bourreille A, Leray V, Gervois N, Rosales C, Ferrier L, Bonnet C, Blottière HM, Galmiche JP. Butyrate inhibits inflammatory responses through NFkappaB inhibition: implications for Crohn’s disease. Gut. 2000;47:397–403. [PMC free article] [PubMed]
84. Aslan A, Triadafilopoulos G. Fish oil fatty acid supplementation in active ulcerative colitis: a double-blind, placebo-controlled, crossover study. Am J Gastroenterol. 1992;87:432–437. [PubMed]
85. Shoda R, Matsueda K, Yamato S, Umeda N. Epidemiologic analysis of Crohn disease in Japan: increased dietary intake of n-6 polyunsaturated fatty acids and animal protein relates to the increased incidence of Crohn disease in Japan. Am J Clin Nutr. 1996;63:741–745. [PubMed]
86. Vilaseca J, Salas A, Guarner F, Rodríguez R, Martínez M, Malagelada JR. Dietary fish oil reduces progression of chronic inflammatory lesions in a rat model of granulomatous colitis. Gut. 1990;31:539–544. [PMC free article] [PubMed]
87. Campos FG, Waitzberg DL, Habr-Gama A, Logullo AF, Noronha IL, Jancar S, Torrinhas RS, Fürst P. Impact of parenteral n-3 fatty acids on experimental acute colitis. Br J Nutr. 2002;87 Suppl 1:S83–S88.[PubMed]
88. Loeschke K, Ueberschaer B, Pietsch A, Gruber E, Ewe K, Wiebecke B, Heldwein W, Lorenz R. n-3 fatty acids only delay early relapse of ulcerative colitis in remission. Dig Dis Sci. 1996;41:2087–2094.[PubMed]
89. Belluzzi A, Brignola C, Campieri M, Pera A, Boschi S, Miglioli M. Effect of an enteric-coated fish-oil preparation on relapses in Crohn’s disease. N Engl J Med. 1996;334:1557–1560. [PubMed]
90. Hawthorne AB, Daneshmend TK, Hawkey CJ, Belluzzi A, Everitt SJ, Holmes GK, Malkinson C, Shaheen MZ, Willars JE. Treatment of ulcerative colitis with fish oil supplementation: a prospective 12 month randomised controlled trial. Gut. 1992;33:922–928. [PMC free article] [PubMed]
91. Hillier K, Jewell R, Dorrell L, Smith CL. Incorporation of fatty acids from fish oil and olive oil into colonic mucosal lipids and effects upon eicosanoid synthesis in inflammatory bowel disease. Gut. 1991;32:1151–1155. [PMC free article] [PubMed]
92. Lehmann JM, Moore LB, Smith-Oliver TA, Wilkison WO, Willson TM, Kliewer SA. An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor gamma (PPAR gamma) J Biol Chem. 1995;270:12953–12956. [PubMed]
93. Lehmann JM, Lenhard JM, Oliver BB, Ringold GM, Kliewer SA. Peroxisome proliferator-activated receptors alpha and gamma are activated by indomethacin and other non-steroidal anti-inflammatory drugs. J Biol Chem. 1997;272:3406–3410. [PubMed]
94. Delerive P, Furman C, Teissier E, Fruchart J, Duriez P, Staels B. Oxidized phospholipids activate PPARalpha in a phospholipase A2-dependent manner. FEBS Lett. 2000;471:34–38. [PubMed]
95. Kliewer SA, Sundseth SS, Jones SA, Brown PJ, Wisely GB, Koble CS, Devchand P, Wahli W, Willson TM, Lenhard JM, et al. Fatty acids and eicosanoids regulate gene expression through direct interactions with peroxisome proliferator-activated receptors alpha and gamma. Proc Natl Acad Sci USA. 1997;94:4318–4323. [PMC free article] [PubMed]
96. Forman BM, Chen J, Evans RM. Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors alpha and delta. Proc Natl Acad Sci USA. 1997;94:4312–4317. [PMC free article] [PubMed]
97. Mansén A, Guardiola-Diaz H, Rafter J, Branting C, Gustafsson JA. Expression of the peroxisome proliferator-activated receptor (PPAR) in the mouse colonic mucosa. Biochem Biophys Res Commun. 1996;222:844–851. [PubMed]
98. Desreumaux P, Ernst O, Geboes K, Gambiez L, Berrebi D, Müller-Alouf H, Hafraoui S, Emilie D, Ectors N, Peuchmaur M, et al. Inflammatory alterations in mesenteric adipose tissue in Crohn’s disease. Gastroenterology. 1999;117:73–81. [PubMed]
99. Su CG, Wen X, Bailey ST, Jiang W, Rangwala SM, Keilbaugh SA, Flanigan A, Murthy S, Lazar MA, Wu GD. A novel therapy for colitis utilizing PPAR-gamma ligands to inhibit the epithelial inflammatory response. J Clin Invest. 1999;104:383–389. [PMC free article] [PubMed]
100. Ricote M, Huang J, Fajas L, Li A, Welch J, Najib J, Witztum JL, Auwerx J, Palinski W, Glass CK. Expression of the peroxisome proliferator-activated receptor gamma (PPARgamma) in human atherosclerosis and regulation in macrophages by colony stimulating factors and oxidized low density lipoprotein. Proc Natl Acad Sci USA. 1998;95:7614–7619. [PMC free article] [PubMed]
101. Staels B, Koenig W, Habib A, Merval R, Lebret M, Torra IP, Delerive P, Fadel A, Chinetti G, Fruchart JC, et al. Activation of human aortic smooth-muscle cells is inhibited by PPARalpha but not by PPARgamma activators. Nature. 1998;393:790–793. [PubMed]
102. Marx N, Bourcier T, Sukhova GK, Libby P, Plutzky J. PPARgamma activation in human endothelial cells increases plasminogen activator inhibitor type-1 expression: PPARgamma as a potential mediator in vascular disease. Arterioscler Thromb Vasc Biol. 1999;19:546–551. [PubMed]
103. Delerive P, Martin-Nizard F, Chinetti G, Trottein F, Fruchart JC, Najib J, Duriez P, Staels B. Peroxisome proliferator-activated receptor activators inhibit thrombin-induced endothelin-1 production in human vascular endothelial cells by inhibiting the activator protein-1 signaling pathway. Circ Res. 1999;85:394–402. [PubMed]
104. Sakai M, Matsushima-Hibiya Y, Nishizawa M, Nishi S. Suppression of rat glutathione transferase P expression by peroxisome proliferators: interaction between Jun and peroxisome proliferator-activated receptor alpha. Cancer Res. 1995;55:5370–5376. [PubMed]
105. Zhou YC, Waxman DJ. STAT5b down-regulates peroxisome proliferator-activated receptor alpha transcription by inhibition of ligand-independent activation function region-1 trans-activation domain. J Biol Chem. 1999;274:29874–29882. [PubMed]
106. Desreumaux P, Dubuquoy L, Nutten S, Peuchmaur M, Englaro W, Schoonjans K, Derijard B, Desvergne B, Wahli W, Chambon P, et al. Attenuation of colon inflammation through activators of the retinoid X receptor (RXR)/peroxisome proliferator-activated receptor gamma (PPARgamma) heterodimer. A basis for new therapeutic strategies. J Exp Med. 2001;193:827–838. [PMC free article] [PubMed]
107. Lewis JD, Lichtenstein GR, Stein RB, Deren JJ, Judge TA, Fogt F, Furth EE, Demissie EJ, Hurd LB, Su CG, et al. An open-label trial of the PPAR-gamma ligand rosiglitazone for active ulcerative colitis. Am J Gastroenterol. 2001;96:3323–3328. [PubMed]
108. Göttlicher M, Widmark E, Li Q, Gustafsson JA. Fatty acids activate a chimera of the clofibric acid-activated receptor and the glucocorticoid receptor. Proc Natl Acad Sci USA. 1992;89:4653–4657.[PMC free article] [PubMed]
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