Impact of Novel Sorghum Bran Diets on DSS-Induced Colitis.

Lauren Ritchie,Nancy Turner,Brad Weeks,Lloyd Rooney,Linda Dykes,Raymond Carroll,Stella Taddeo

doi:10.3390/nu9040330

Abstract

We have demonstrated that polyphenol-rich sorghum bran diets alter fecal microbiota; however, little is known regarding their effect on colon inflammation. Our aim was to characterize the effect of sorghum bran diets on intestinal homeostasis during dextran sodium sulfate (DSS)-induced colitis. Male Sprague-Dawley rats (N = 20/diet) were provided diets containing 6% fiber from cellulose, or Black (3-deoxyanthocyanins), Sumac (condensed tannins) or Hi Tannin Black (both) sorghum bran. Colitis was induced (N = 10/diet) with three separate 48-h exposures to 3% DSS, and feces were collected. On Day 82, animals were euthanized and the colon resected. Only discrete mucosal lesions, with no diarrhea or bloody stools, were observed in DSS rats. Only bran diets upregulated proliferation and Tff3, Tgfβ and short chain fatty acids (SCFA) transporter expression after a DSS challenge. DSS did not significantly affect fecal SCFA concentrations. Bran diets alone upregulated repair mechanisms and SCFA transporter expression, which suggests these polyphenol-rich sorghum brans may suppress some consequences of colitis.

Highlights

Inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis (UC), affects nearly 1.4 million people in the United States [1]
We hypothesized that feeding sorghum bran diets would attenuate the effects of dextran sodium sulfate (DSS)-induced UC
Diets rich in fiber have been shown to reduce the risk of developing gastrointestinal disorders [29,37]

Summary

Introduction

Inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis (UC), affects nearly 1.4 million people in the United States [1]. The complete etiology of UC is not fully understood, recent research has indicated that perturbations in host immune response to intestinal microbiota could be a major factor in the progression of this disease [2,3]. The intestinal microbiota plays a role in host health by affecting the luminal environment and interacting with host epithelial cells. Microbial impacts on health can be derived from fermentation of dietary fiber, alteration of intestinal motility and pH, as well as protection against invading pathogens. Fermentation of dietary fiber produces metabolites including short chain fatty acids (SCFA), such as butyrate, which is the preferred fuel source for colonocytes [6,7]. The microbiota affects host innate immunity by signaling through toll-like receptors (TLR) and the nuclear factor-κB (NF-κB) pathway [4,12]. Dysregulation of the TLR pathway has been associated with the progression of intestinal inflammation and the pathogenesis of UC [4,12]

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