Dietary fat has several essential functions in the human body. First, it functions as a supply of energy and structural components for the cells and second, it functions as a regulator of gene expression, which influences lipid, carbohydrate, and protein metabolism, along with cell growth and differentiation. The effects of fatty acids on gene expression are cell-specific and influenced by structure and metabolism. Fatty acids interact with the genome. They regulate PPAR, and the activity or nuclear abundance like SREBP. Fatty acids bind directly with one another to regulate gene expression.
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Alternately, fatty acids behave on gene expression through their effects on specific enzyme-mediated pathways, such as cyclooxygenase, lipoxygenase, protein kinase C, or sphingomyelinase signal transduction pathways, or through pathways that require changes in tissue lipid to lipid raft composition which affect G-protein receptor or tyrosine kinase-linked receptor signaling. Additional definition of these fatty acid-regulated pathways can offer insight into the role dietary fat plays in human health as well as the beginning and growth of many chronic diseases, such as coronary artery disease and atherosclerosis, dyslipidemia and inflammation, obesity and diabetes, cancer, major depressive disorders, and schizophrenia. The effects of fatty acids on gene expression, however, have been widely described on inflammatory bowel disease, or IBD.
The effect of fatty acids on gene expression was previously determined to result mainly from changes in tissue phospholipids or eicosanoid production. More recently, the discovery of nuclear receptors; such as peroxisome proliferator-activated receptors, or PPARs, and their regulation by fatty acids, has significantly altered this view. PPARs are ligand activated transcription factors that upon heterodimerization with the retinoic X receptor, or RXR, comprehend PPAR response elements in the promoter regions of different genes, that have an impact on gene transcription. PPARs bind various ligands, including nonsteroidal anti inflammatory medications, or NSAIDS, thiazolidinediones (antidiabetic agents) along with PUFAs and their metabolites. Several subtypes of the receptor are recognized (α,δ,γ) and are expressed in several different cells. PPARγ is extracted from the adrenal gland, with most of its numbers observed in the colon.
PPARγ has been implicated in the regulation of inflammation, and it has become a potential therapeutic goal in treating inflammatory diseases, such as IBD. It has been suggested that people with ulcerative colitis, or UC, have a mucosal deficit in PPARγ that could bring about the development of their own disease. Analysis of the mRNA and proteins within colonic biopsies demonstrated decreased levels of PPARγ in UC patients in comparison with Crohn’s patients or healthy subjects.
Using colon cancer lines, it has been demonstrated that PPAR ligands attenuate cytokine gene expression by inhibiting NF-κB via an IκB determined mechanism. Further research studies imply that PPAR activators inhibit COX2 by interruption with NF-κB. PPARs impair interactions with STAT and other signaling pathways as well as the AP-1 signaling pathway.
Animal studies support using PPAR for autoimmune inflammation. Inflammation decreased by ligands for PPAR. The direction of PPAR and RXR agonists synergistically reduced TNBS-induced colitis, together with improved macroscopic and histologic scores, reductions in TNFα and IL-1β mRNA, and diminished NF-κB DNA binding actions. Though clinical evidence is limited, the results of an open source research study with rosiglitazone, a PPARγ ligand as therapy for UC, demonstrated that 27 percent of patients achieved remission after 12 weeks of therapy. Thus, PPARγ ligands may represent a cure for UC, where double-blind, placebo-controlled, randomized trials have been warranted.
Of substantial curiosity, the capability to regulate PPAR nutritionally has been examined. Dietary PUFA demonstrated an impact during the regulation of transcription factors on gene expression. Fatty acid regulation of PPAR was originally detected by Gottlicher et al.. A choice of fatty acids, like eicosanoids, and metabolites are proven to activate PPAR. Both PPARα and PPARγ bind mono- and polyunsaturated fatty acids. Thus, the anti inflammatory effects of n3 PUFA may entail PPAR and its interruption with NFκB, rather than only changes in eicosanoid synthesis.
Fatty acids regulate gene expression involved in lipid and energy metabolism. Polyunsaturated fatty acids, or PUFA, though not saturated or polyunsaturated FA, suppress the induction of lipogenic genes by inhibiting their expression and processing of SREBP-1c. This impact of PUFA suggests that SREBP-1c may regulate the synthesis of fatty acids to glycerolipids, among others. PPARalpha has a role in the adaptation to fasting by inducing ketogenesis in mitochondria. During fasting, fatty acids are considered as ligands of PPARalpha. Dietary PUFA, except for 18:2 n-6, are extremely prone to induce fatty acid oxidation enzymes through PPARalpha because of specific mechanisms. Signaling functions of PPARalpha pPARalpha is needed for controlling the synthesis of fatty acids. Further research is needed to conclude the full effects of fatty acids in relation to the regulation of transcription factors for gene expression in inflammatory bowel disease, or IBD.
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By Dr. Alex Jimenez
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, RodrÃguez R, MartÃnez 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]
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.
Professional Scope of Practice *
The information herein on "Regulation of Gene Expression by Fatty Acids for IBD" is not intended to replace a one-on-one relationship with a qualified health care professional or licensed physician and is not medical advice. We encourage you to make healthcare decisions based on your research and partnership with a qualified healthcare professional.
Blog Information & Scope Discussions
Our information scope is limited to Chiropractic, musculoskeletal, physical medicines, wellness, contributing etiological viscerosomatic disturbances within clinical presentations, associated somatovisceral reflex clinical dynamics, subluxation complexes, sensitive health issues, and/or functional medicine articles, topics, and discussions.
We provide and present clinical collaboration with specialists from various disciplines. Each specialist is governed by their professional scope of practice and their jurisdiction of licensure. We use functional health & wellness protocols to treat and support care for the injuries or disorders of the musculoskeletal system.
Our videos, posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate to and directly or indirectly support our clinical scope of practice.*
Our office has reasonably attempted to provide supportive citations and has identified the relevant research study or studies supporting our posts. We provide copies of supporting research studies available to regulatory boards and the public upon request.
We understand that we cover matters that require an additional explanation of how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez, DC, or contact us at 915-850-0900.
We are here to help you and your family.
Blessings
Dr. Alex Jimenez DC, MSACP, RN*, CCST, IFMCP*, CIFM*, ATN*
email: coach@elpasofunctionalmedicine.com
Licensed as a Doctor of Chiropractic (DC) in Texas & New Mexico*
Texas DC License # TX5807, New Mexico DC License # NM-DC2182
Licensed as a Registered Nurse (RN*) in Florida
Florida License RN License # RN9617241 (Control No. 3558029)
Compact Status: Multi-State License: Authorized to Practice in 40 States*
Presently Matriculated: ICHS: MSN* FNP (Family Nurse Practitioner Program)
Dr. Alex Jimenez DC, MSACP, RN* CIFM*, IFMCP*, ATN*, CCST
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