Dietary fiber fraction of germinated barley foodstuff attenuated mucosal damage and diarrhea, and accelerated the repair of the colonic mucosa in an experimental colitis.
ABSTRACT Germinated barley foodstuff (GBF) contains protein and insoluble dietary fiber. We have previously shown in ulcerative colitis patients and a colitis model that GBF feeding attenuates mucosal damage by increasing luminal butyrate levels. However, the detailed mechanism remains unclear because of its heterogeneous nature. The present study was carried out to: (i) evaluate the active ingredient in GBF; and (ii) examine its effect on the repair process in colonic inflammation by using a dextran sulfate sodium (DSS) colitis model.
Colitis was induced by feeding a diet containing 0.5-3.5% DSS to male Sprague-Dawley rats. (i) Active ingredient: GBF was fractionated enzymatically into fiber- and protein-rich fractions. Each fraction was administered to DSS-colitis rats. Clinical signs, cecal short chain fatty acid concentrations and serum alpha1-acid glycoprotein (AAG) levels were determined. (ii) Effect on mucosal repair: GBF with or without salazosulfapyridine (SASP), or SASP alone was administered to rats after the onset of colitis. Seven days after initial treatment, the number of epithelial cells in HE sections was evaluated morphologically in a blind fashion and serum AAG was determined.
(i) Germinate barley foodstuff and GBF-fiber significantly attenuated the clinical signs of colitis and decreased serum AAG levels, with a significant increase in cecal butyrate production, while GBF-protein did not. (ii) Treatment with GBF alone and GBF plus SASP significantly accelerated colonic epithelial repair and improved clinical signs.
These findings suggest that the fiber fraction of GBF may effectively enhance luminal butyrate production, and thereby accelerate colonic epithelial repair in colitis.
- Journal of Pharmacological Sciences 01/2005; 99(4):329-334. · 2.11 Impact Factor
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ABSTRACT: One explanation for the increased incidence of allergies, asthma, and even some autoimmune diseases has been the hygiene hypothesis. However, recent studies also highlight an important role for diet and bacterial metabolites in controlling various immune pathways, including gut and immune homeostasis, regulatory T cell biology, and inflammation. Dietary-related metabolites engage "metabolite-sensing" G-protein-coupled receptors, such as GPR43, GPR41, GPR109A, GPR120, and GPR35. These receptors are expressed on immune cells and some gut epithelial cells and generally mediate a direct anti-inflammatory effect. Insufficient intake of "healthy foodstuffs" adversely affects the production of bacterial metabolites. These metabolites and those derived directly from food drive beneficial downstream effects on immune pathways. We propose that insufficient exposure to dietary and bacterial metabolites might underlie the development of inflammatory disorders in Western countries. This review highlights what is currently known about diet, metabolites, and their associated immune pathways in relation to the development of inflammatory disease.Immunity 06/2014; 40(6):833-842. · 19.75 Impact Factor