Cereals and Legumes in Nutrition of People with Celiac Disease

Zuzana Mlyneková¹, Mária Chrenková^1, and Zuzana Formelová¹

¹Research Institute of Animal Production Nitra, 951 41, Department of Nutrition, Slovak Republic

Cite this paper:
Zuzana Mlyneková, Mária Chrenková and Zuzana Formelová. Cereals and Legumes in Nutrition of People with Celiac Disease. International Journal of Celiac Disease. 2014; 2(3):105-109. doi: 10.12691/ijcd-2-3-3

Abstract

Cereals and legumes rank among the most important group of crop plant production. The aim of this paper was to point out the suitability of cereals and legumes in the diet of people living with an autoimmune disease of the small intestine, the celiac disease. Cereals match the best current ideas of healthy and balanced diet and provide decisive part of the energy intake from food in human nutrition and no small share from the total protein intake. Some cereals contain celiac active polypeptides and in susceptible individuals cause allergic reactions. Celiac active ingredients are found in the prolamin fraction. If the content of prolamine is in an amount of 4-8%, the products can be considered appropriate for the celiac diet. Wheat, barley, rye and oat should be excluded from the diet, if a person has confirmed celiac disease. On a worldwide basis, legumes contribute to about one-third of humankind's direct protein intake. Legumes also accumulate natural products (secondary metabolites) such as isoflavonoids that are considered beneficial to human health through anticancer and other health-promoting activities. The biggest advantage of legumes is that they are gluten-free and are suitable for gluten-free diet.

Keywords:
cereals legumes celiac disease

This work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

References:

[1]	Andoh A, Bamba S, Fujiyama Y, Brittan M, Wright NA. Colonic subepithelial myofibroblasts in mucosal inflammation and repair: contribution of bone marrow-derived stem cells to the gut regenerative response. J Gastroenterol 2005; 40: 1089-1099.
[2]	Briani C, Samaroo D, Alaedini A. Celiac disease: from gluten to autoimmunity. Autoimmun Rev 2008; 7: 644-650.
[3]	Brittan M, Hunt T, Jeffery R, Poulsom R, Forbes SJ, Hodivala- Dilke K, Goldman J, Alison MR, Wright NA. Bone marrow derivation of pericryptal myofibroblasts in the mouse and human small intestine and colon. Gut 2002; 50: 752-757.
[4]	Catassi C, Fasano A. Celiac disease. Curr Opin Gastroenterol 2008; 24: 687-691.
[5]	Ciccocioppo R, Di Sabatino A, Bauer M, Della Riccia DN, Bizzini F, Biagi F, Cifone MG, Corazza GR, Schuppan D. Matrix metalloproteinase pattern in celiac duodenal mucosa. Lab invest 2005; 85: 397-407.
[6]	Daum S, Bauer U, Foss HD, Schuppan D, Stein H, Riecken EO, Ullrich R. Increased expression of mRNA for matrix metalloproteinases-1 and -3 and tissue inhibitor of metalloproteinases-1 in intestinal biopsy specimens from patients with coeliac disease. Gut 1999; 44: 17-25.
[7]	De Wever O, Demetter P, Mareel M, Bracke M. Stromal myofibroblasts are drivers of invasive cancer growth. Int J Cancer. 2008; 123: 2229-2238.
[8]	Dieterich W, Ehnis T, Bauer M, Donner P, Volta U, Riecken EO, Schuppan D. Identification of tissue transglutaminase as the autoantigen of celiac disease. Nat Med 1997; 3: 797-801.
[9]	Elli L, Bardella MT. Motility disorders in patients with celiac disease. Scand J Gastroenterol 2005; 40: 743-749.
[10]	Elli L, Bergamini CM, Bardella MT, Schuppan D. Transglutaminases in inflammation and fibrosis of the gastrointestinal tract and the liver. Dig Liver Dis 2009 41: 541-550.
[11]	Eyden B. The myofibroblast: phenotypic characterization as a prerequisite to understanding its functions in translational medicine. J Cell Mol Med 2008; 12: 22-37.
[12]	Guandalini S, Assiri A. Celiac Disease: A Review. JAMA pediatr 2014; 168: 272-278.
[13]	Halttunen T, Maki M. Serum immunoglobulin A from patients with celiac disease inhibits human T84 intestinal crypt epithelial cell differentiation. Gastroenterology 1999; 116: 566-572.
[14]	Hinz B, Phan SH, Thannickal VJ, Galli A, Bochaton-Piallat ML, Gabbiani G. The myofibroblast: one function, multiple origins. Am J Pathol 2007; 170: 1807-1816.
[15]	Klein S, Seidler B, Kettenberger A, Sibaev A, Rohn M, Feil R, Allescher HD, Vanderwinden JM, Hofmann F, Schemann M, Rad R, Storr MA, Schmid RM, Schneider G, Saur D. Interstitial cells of Cajal integrate excitatory and inhibitory neurotransmission with intestinal slow-wave activity. Nat Commun 2013; 4: 1630.
[16]	MacDonald TT, Monteleone I, Fantini MC, Monteleone G. Regulation of homeostasis and inflammation in the intestine. Gastroenterology 2011; 140: 1768-1775.
[17]	Marastoni S, Ligresti G, Lorenzon E, Colombatti A, Mongiat M. Extracellular matrix: a matter of life and death. Connect Tissue Res 2008; 49: 203-206.
[18]	McLin VA, Henning SJ, Jamrich M. The role of the visceral mesoderm in the development of the gastrointestinal tract. Gastroenterology 2009; 136: 2074-2091.
[19]	Medina C, Radomski MW. Role of matrix metalloproteinases in intestinal inflammation. J Pharmacol Exp Ther 2006; 318: 933-938.
[20]	Nelson AR, Fingleton B, Rothenberg ML, Matrisian LM.. Matrix metalloproteinases: biologic activity and clinical implications. J Clin Oncol 2000; 18: 1135-1149.
[21]	Okuno T, Andoh A, Bamba S, Araki Y, Fujiyama Y, Fujiyama M, Bamba T. Interleukin-1beta and tumor necrosis factor-alpha induce chemokine and matrix metalloproteinase gene expression in human colonic subepithelial myofibroblasts, Scand J Gastroenterol 2002; 37: 317-324.
[22]	Polyak K, Weinberg RA. Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits Nat Rev Cancer 2009; 9: 265-273.
[23]	Powell DW, Mifflin RC, Valentich JD, Crowe SE, Saada JI, West AB. Myofibroblasts. II. Intestinal subepithelial myofibroblasts. Am J Physiol 1999; 277: C183-201.
[24]	Powell DW, Pinchuk IV, Saada JI, Chen X, Mifflin RC. Mesenchymal cells of the intestinal lamina propria.. Annu Rev Physiol 2011; 73: 213-237.
[25]	Roncoroni L, Elli L, Bardella MT, Perrucci G, Ciulla M, Lombardo V, Tomba C, Conte D, Doneda L. Extracellular matrix proteins and displacement of cultured fibroblasts from duodenal biopsies in celiac patients and controls. J Transl Med 2013; 11: 91.
[26]	Sanders KM, Koh SD, Ward SM. Interstitial cells of cajal as pacemakers in the gastrointestinal tract. Annu Rev Physiol 2006; 68: 307-343.
[27]	Sanders KM, Ward SM. Interstitial cells of Cajal: a new perspective on smooth muscle function. J Physiol 2006; 576: 721- 726.
[28]	Sappino AP, Dietrich PY, Skalli O, Widgren S, Gabbiani G. Colonic pericryptal fibroblasts. Differentiation pattern in embryogenesis and phenotypic modulation in epithelial proliferative lesions. Virchows Archiv A Pathol Ana Histopathol 1989; 415: 551-557.
[29]	Simmons JG, Pucilowska JB, Keku TO, Lund PK. IGF-I and TGF-beta1 have distinct effects on phenotype and proliferation of intestinal fibroblasts. Am J Physiol Gastrointest Liver Physiol 2002; 283: G809-818.
[30]	Simon-Assmann P, Kedinger M, De Arcangelis A, Rousseau V, Simo P. Extracellular matrix components in intestinal development. Experientia 1995; 51: 883-900
[31]	Sziksz E, Pap D, Veres G, Fekete A, Tulassay T, Vannay A. Involvement of heat shock proteins in gluten-sensitive enteropathy. World J Gastroenterol 2014; 20: 6495-6503.
[32]	Sziksz E, Vörös P, Veres G, Fekete A, Vannay Á. Coeliac Disease: From Triggering Factors to Treatment. International Journal of Celiac Disease 2013; 1: 9-13
[33]	Trier JS. Celiac sprue. N Eng J Med 1991; 325: 1709-1719.
[34]	Verbeke S, Gotteland M, Fernandez M, Bremer J, Rios G, Brunser O. Basement membrane and connective tissue proteins in intestinal mucosa of patients with coeliac disease. J Clin Pathol 2002; 55: 440-445.
[35]	Yasui H, Andoh A, Bamba S, Inatomi O, Ishida H, Fujiyama Y. Role of fibroblast growth factor-2 in the expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases in human intestinal myofibroblasts. Digestion 2004; 69: 34-44.
[36]	Zemskov EA, Janiak A, Hang J, Waghray A, Belkin AM. The role of tissue transglutaminase in cell-matrix interactions. Front Biosci 2006; 11: 1057-1076.