Deneysel Ülseratif Kolit Üzerine Yüksek Karbonhidratlı, Yüksek Yağlı ve Aralıklı Beslemenin Etkisi

Year 2018, Volume: 7 Issue: 1, 7 - 14, 04.07.2018

Ahmet Uyar , Hüseyin Emlik Turan Yaman

https://doi.org/10.31196/huvfd.458770

Cited By: 2

Abstract

Bu
çalışmada, dünyada görülme sıklığı artan inflamatuvar bağırsak hastalıklarının
(İBH) bir tanesi olan Ülseratif kolit (ÜK) hastalığının Wistar albino türü
ratlarda deneysel oluşumu üzerine beslenme şekli ve sıklığının karşılaştırmalı
olarak araştırılması amaçlanmıştır. Bu amaçla; Kontrol (n=7), Kolit (n=7),
Kolit-Yüksek Karbonhidratlı Diyet (K-YKD) (n=7), Kolit–Yüksek Karbonhidratlı
Aralıklı Diyet (K-YKAD) (n=7), Kolit–Yüksek Yağlı Diyet (K-YYD) (n=7), Kolit-Yüksek
Yağlı Aralıklı Diyet (K-YYAD) (n=7) olacak şekilde çalışma grupları
oluşturuldu. Gruplardan aralıklı besleme gruplarına haftada sadece 2 gün (ardarda
olmayan) diyet verilmesine 24 saat ara verildi. 7 haftalık beslemeden sonra deneysel
kolit modeli; kolit ve tedavi gruplarındaki (Kolit, K-YKD, K-YKAD, K-YYD,
K-YYAD) ratlara anestezi altında 30^o trendelenburg pozisyonunda 8
mm’lik kateterin rektal yoldan 8 cm ileriye asetik asidin (pH 2.4, % 4)
intrarektal (i.r.) olarak uygulanması ile oluşturuldu. 72 saat sonra ratlar
sakrifiye edilerek histopatolojik örnekler %10 tamponlu formaldehite alındı. Histopatolojik
incelemelere göre asetik asitin ciddi kolit hasarlarına neden olduğu buna
karşın aralıklı olarak verilen diyet gruplarında bu hasarların oldukça minimal
düzeyde kaldığı görülmüştür. Sonuç olarak kolit modelinde aralıklı diyet
uygulamasının olumlu etkileri olduğu kanısına varıldı. 

Keywords

Yüksek Karbonhidratlı, Yağlı ve Aralıklı Diyet, Kolit, Rat

Effect of High Carbohydrate, Fat and Intermittent Fasting Diet on Experimental Ulcerative Colitis

Abstract

In this study, it was aimed to comparatively investigate the effect of  diet type and feeding frequency on occurence of experimental ulcerative colitis (UC), in Wistar albino rats. For this purpose, 7 rats were randomly selected and 6 groups were formed as Control (n=7), Colitis (n=7), Colitis-High Carbohydrate Diet (C-HCD) (n=7), Colitis - High Carbohydrate Diet with Intermittent Feeding (C-HCIFD) (n=7), Colitis -High Fat Diet (C-HFD) (n=7), Colitis-High Fat Diet with Intermittent Feeding (C-HFIFD) (n=7). In intermittent feeding groups the feeding  was interrupted twice in a week for 24 hours . After 7 weeks of feeding, experimental colitis model was induced in colitis and treatment groups rats by intrarectal administration of acetic acid (pH 2.4, 4 %). After the 72 hours rats were sacrificed and colon samples were taken into 10% formalin solution. Histopathological studies have shown that acetic acid caused severe colitis damage, whereas the damage remained at minimal levels in groups with intermittent feeding. As a result, it was concluded that intermittent feeding administration in the colitis model had positive effects.

Keywords

High Carbohydrate, Fat and Intermittent Fasting Diet, Colitis, Rat

References

• Akman C, Zhao Q, Liu X, Holmes GL, 2004. Effect of food deprivation during early development on cognition and neurogenesis in therat. Epilepsy and Behavior, 5, 446–454.
• Ananthakrishnan AN, Khalili H, Konijeti GG, Higuchi LM, de Silva P, Korzenik JR, Fuchs CS, Willett WC, Richter JM, Chan AT, 2013: A prospective study of long-term intake of dietary fiber and risk of Crohn’s disease and ulcerative colitis. Gastroenterology, 145 (5): 970-7.
• Ananthakrishnan AN, Khalili H, Konijeti GG, Higuchi LM, de Silva P, Fuchs CS, Willett WC, Richter JM, Chan AT, 2014: Long-term intake of dietary fat and risk of ulcerative colitis and crohn’s diseas. Gut, 63 (5), 776–784.
• Appleyard CB, Wallace JL, 1995: Reactivation of hapten-induced colitis and its prevention by anti-inflammatory drugs. Am J Physiol, 269, 119-25.
• Aslan A, Polat G, Atik E, Temiz M, Bağdatoğlu ÖT, Aban N, 2008: Deneysel ülseratif kolitte selenyumun etkinliği. Mersin Üniv Sağlık Bilim Derg, 1 (2), 7-11.
• Chan SS, Luben R, van Schaik F, Oldenburg B, Bueno-deMesquita HB, Hallmans G, Karling P, Lindgren S, Grip O, Key T, Crowe FL, Bergmann MM, Overvad K, Palli D, Masala G, Khaw KT, Racine A, Carbonnel F, Boutron-Ruault MC, Olsen A, Tjonneland A, Kaaks R, Tumino R, Trichopoulou A, Hart AR, 2014: Carbohydrate intake in the etiology of Crohn’s disease and ulcerative colitis. Inflamm Bowel Dis, 20, 2013-2021.
• Chapman-Kiddell CA, Davies PS, Gillen L, Radford-Smith GL, 2010: Role of diet in the development of inflammatory bowel disease. Inflamm Bowel Dis, 16, 137-151.
• Cope G, 2015: Overview of dietary choices for ulcerative colitis and Crohn’s disease. Gastrointestinal Nursing, 13,1, 33-37.
• Cross SS, Harison RF, 2002: Discriminant histological feature in the diagnosis of chronic idiopathic inflammatory bowel disease: analysis of a large dataset by a novel data visualisation technique. J Clin Pathol, 55, 51-7.
• Daneshmand A, Mohammadi H, Rahimian R, 2011: Chronic lithium administration ameliorates 2, 4, 6‐trinitrobenzene sulfonic acid‐induced colitis in rats; potential role for adenosine triphosphate sensitive potassium channels. J Gastroenterol Hepatol, 26 (7), 1174-1181.
• Dieleman LA, Ridwan BU, Tennyson GS, 1994: Dextran sulfate sodium-induced colitis occurs in severe combined immunodeficient mice. Gastroenterology, 107, 1643-52.
• Ewaschuk, J.B. ve Dieleman, L.A., 2006. Probiotics and prebiotics in chronic inflammatory bowel dis-eases. World J Gastroenterol, 12 (37), 5941-5950.
• Galvez J, Coelho G, Crespo ME, Cruz T, Rodriguez-Cabezas ME, Concha A, 2001: Intestinal anti-inflammatory activity of morin on chronic experimental colitis in the rat. Aliment Pharmacol Ther, 15, 2027-39.
• Griffiths AM, Buller HB, 2000: Inflammatory Bowel Disease In: Pediatric Gastrointestinal Disease. Eds: Walker, Durie, Hamilton, 3rd ed,: B.C. Decker Inc, Ontario, p. 613- 52.
• Gruber L, Kisling S, Lichti P, Martin FP, May S, Klingenspor M, Lichtenegger M, Rychlik M, Haller D, 2013: High fat diet pathogenesis of murine Crohn’s disease-like ileitis independently of obesity. PLoS One, 8(8), e71661.
• Gulhane M, Murray L, Lourie R, Tong H, Sheng YH, Wang R, Kang A, Schreiber V, Wong KY, Magor G, Stuart D, Begun J, Florin TH, Perkins A, Cuív PÓ, McGuckin MA, Hasnain SZ, 2016: High fat diets induce colonic epithelial cell stress and inflammation that is reversed by IL-22. Scientific Reports, 6, 28990.
• Hagar H, Medany A, Eter E, 2007: Ameliorative effect of pyrrolidinedithiocarbamate on acetic acid-induced colitis in rats. Eur J Pharmacol, 554, 69–77.
• Hagopian K, 2005: Krebs cycle enzymes from livers of old mice are differantially regulated by caloric restriction. Phsiol and Behavior, 85, 581-592.
• Hansen TS, Jess T, Vind I, Elkjaer M, Nielsen MF, Gamborg M, Munkholm P, 2011: Environmental factors in inflammatory bowel disease: a case-control study based on a Danish inception cohort. J Crohns Colitis, 5, 577-584.
• Hopfer U, 1997: Digestion and Absorbtion of Basic Nutritional ConstituentsIn: Devlin Thomas M, Editor. Textbook of Biochemistry with Clinical Correlations 4th ed. New York: Von Hoffmann Press, p. 1056-1083.
• Hou JK, Abraham B, El-Serag H, 2011: Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Am J Gastroenterol, 106(4), 563-573.
• Jakobsen C, Paerregaard A, Munkholm P, Wewer V, 2013: Environmental factors and risk of developing paediatric inflammatory bowel disease -- a population based study 2007-2009. J Crohns Colitis, 7, 79-88.
• Kumar V, Abbas K.A, Fausto M, 2007: Robbinson's Basic Pathology 8. Edition. 612-616.
• Maconi G, Ardizzone S, Cucino C, Bezzio C, Russo AG, Bianchi Porro G, 2010: Pre-illness changes in dietary habits and diet as a risk factor for inflammatory bowel disease: a case-control study. World J Gastroenterol, 16, 4297-4304.
• Lam YY, Ha CW, Campbell CR, Mitchell AJ, Dinudom A, Oscarsson J, Cook DI, Hunt NH, Caterson ID, Holmes AJ, Storlien LH, 2012: Increased gut permeability and microbiota change associate with mesenteric fat inflammation and metabolic dysfunction in diet-induced obese mice. PLoS One 7(3): e34233. doi:10.1371/journal.pone.0034233.
• Longo VD, Panda S, 2016: Fasting, circadian rhythms, and time-restricted feding in healthy lifespan. Cell Metab, 23, 1048–1059.
• Malafaia AB, Nassif PAN, Ribas CAPM, Ariede BL, Sue KN, Cruz MA, 2013: Obesity Induction With High Fat Sucrose In Rats. ABCD Arq Bras Cir Dig, 26, 1, 17-21.
• Masoro EJ, 2001: Physiology of aging. Int J Sport Nutr Exerc Metab, 218-22.
• Merry BJ, 2005: Dietary restriction in rodents- delayed or retarded ageing? Mech Aging Dev,126, 951-959.
• Montrose DC, Horelik NA, Madigan JP, Stoner GD, Wang LS, Bruno RS, Park HJ, Giardina C, Rosenberg DW, 2011: Anti-inflammatory effects of freeze-dried black raspberry powder in ulcerative colitis. Carcinogenesis, 32 (3), 343-350.
• Morris GP, Beck PL, Herridge MS, Depew WT, Szewczuk MR, 1989: Hapten-induced model of chronic inflammation and ulceration in the rat colon. Gastroenterology, 96 (3), 795-803.
• Nagib MM, Tadros MG, ELSayed MI, Khalifa AE,2013:Anti-inflammatory and anti-oxidant activities of olmesartan medoxomil ameliorate experimental colitis in rats. Toxicol Appl Pharmacol, 271 (1),106-113.
• Obermeier F. Kojouharoff G, 1999: Interferon–gamma (IFN-ɤ)-and tumour necrosis factor (TNF)-induced nitric oxide as toxic effector molecule in chronic dextran sulphate sodium (DSS)-induced colitis in mice. Clin Exp Immunol, 116, 238-245.
• Okada T, Otsubo T, Hagiwara T, Inazuka F, Kobayashi E, Fukuda S, Inoue T, Higuchi K, Kawamura YI, Dohi T, 2017: Intermittent fasting prompted recovery from dextran sulfate sodium_induced colitis in mice. J Clin Biochem Nutr, 61, 2, 100–107.
• Ordás I, Eckmann L, Talamini M, Baumgart DC, Sandborn WJ, 2012: Ulcerative colitis. Lancet, 380, 1606-1619.
• Özgün E, Özgün GS, Eskiocak S, Yalçın Ö ve Gökmen SS, 2013: Effect of L-carnitine on serum paraoxonase, arylesterase and lactonase activities and oxidative status in experimental colitis. Turk J Biochem, 38 (2), 145–153.
• Öztürk Ç, 2013: Nesfatin-1’in sıçanda asetik asit ile indüklenmiş kolitte anti-inflamatuvar etkisi ve altta yatan mekanizma. Yüksek Lisans Tezi, MU Sağlık Bilimleri Enstitüsü, İstanbul.
• Özütemiz AÖ, Ünsal B, Alkanat M, Aksöz K, Dinçer Ç ve Batur Y, 1997: Sıçanlardaki asetik asit kolitinde diltiazemin etkisi. Turk J Gastroenterol, 8, 300-3004.
• Patterson RE, Laughlin GA, Sears DD, LaCroix AZ, Marinac C, Gallo LC, Hartman SJ, Natarajan L, Senger CM, Martínez ME, and Villaseñor A, 2015: Intermittent Fasting And Human Metabolic Healt. J Acad Nutr Diet, 115 (8), 1203–1212.
• Podolsky DK, 2009: Inflammatory bowel disease. N Engl Med, 347 (6), 417-29.
• Rame LT, Hart RW, Leakey JEA, 1998: Calorie restriction as a mechanism mediating resistance to environmental disease. Environ. Health Perspect, 106, 313–324.
• Reif S, Klein I, Lubin F,1997: Pre-illness dietary factors in inflammatory bowel disease. Gut, 40, 754-60.
• Reiser K, Mcgee C, Rucker R, Mcdonald R, 1995: Effect of aging and caloric restriction on extracellular-matrix biosynthesis in a model of injury repair in rats. J of Geront Series A- Biol Sci.and Med Sci, 50, B40-B47.
• Riordan AM, Ruxton CH, Hunter JO, 1998: A review of associations between Crohn‘s disease and consumption of sugars. Eur J Clin Nutr, 52, 229-238.
• Sakamoto N, Kono S, Wakai K, 2005: Dietary risk factors for inflammatory bowel disease: a multicenter case-control study in Japan. Inflamm Bowel Dis, 11, 154-63.
• Savendahl L, Underwood LE, Haldeman KM, Ulshen MH, Lund PK, 1997: Fasting prevents experimental murine colitis produced by dextran sulfate sodium and decreases interleukin-1 and insulin-like growth factor-1 messenger ribonucleic acid. Endocrinology, 138, 734–740.
• Schrauwen P, Westerterp KR, 2000: The role of high-fat diets and physical activity in the regulation of body weight. Br J Nutr, 84 (4), 417-27.
• Speakman JR, Mitchell SE, 2011: Caloric restriction. Molec Aspects of Med, 32, 159-221.
• Teixeira LG, Leonel AJ, Aguilar EC, Batista NV, Alves AC, Coimbra CC, Ferreira AV, de Faria AM, Cara DC, Alvarez Leite JI, 2011:The combination of high-fat diet-induced obesity and chronic ulcerative colitis reciprocally exacerbates adipose tissue and colon inflammation. Lipids Health Dis, 10, 204.
• Thornton JR, Emmett PM, Heaton KW,1979: Diet and Crohn's disease: characteristics of the pre-illness diet. Br Med J, 2, 762-4.
• Torres MI, Garcia-Martin M, Fernandez MI, Nieto N, Gil A, Rios A, 1999: Experimental colitis induced by trinitrobenzenesulfonic acid: an ultrastructural and histochemical study. Dig Dis Sci, 44, 2523-9.
• Tragnone A, Valpiani D, Miglio F, 1995: Dietary habits as risk factors for inflammatory bowel disease. Eur J Gastroenterol Hepatol, 7, 47-51.
• Troyer DA, Venkatraman JT, Fernandes G, 1998: Effects of calorie restriction and ω-3 dietary fat on aging in short- and long-lived rodents. Age, 21, 175–182.
• Uygun A, Saka M, 2005: Spesifik gastrointestinal sistem hastalıklarında beslenme. Güncel Gastroenteroloji, 9 (2), 145-155.
• Yıldırım B,Tuncer C, Şahin D, Dinçel AS, Göçün FPU, Leventoğlu S, Sancak S, Altan N, Dursun A, 2014: Effect of colchicine on experimental acetic acid induced colitis, Turk J Biochem, 39 (1), 63–69.
• Yılmaz A, Eskiocak S, Altaner Ş, Turan N, 2010: Asetik asitle Kolit Geliştirilen Sıçanlarda N-asetilsisteinin Protein Oksidasyonuna Etkisi. J Turk Clin Biochem, 8(1), 23-33.
• Zhou X, J De Schepper, D De Craemer, M Delhase, G Gys, J Smitz, E L Hooghe Peters, 1998: Pituitary growth hormone release and gene expression in cafeteria-diet-induced obese rats. J Endocrinol, 159, 165–172.