Plain language summary
Colorectal cancer (CRC) is the third most common cancer in the world. Rice bran is high in phytochemicals, fibre and other bioactive compounds that may have potential to reduce cancer formation. Rice bran consumption has been shown to reduce CRC growth in mice, as well as alter the stool microbiome in humans. This alteration of the gut microbiome and the metabolic end products produced by it is thought to provide positive health benefits in terms of CRC development. This randomised controlled trial with CRC survivors included daily consumption of 30g/day of rice bran for 28 days in the intervention group, consisting of 9 participants. No rice bran was consumed in the control group of 10 participants. The aim of the study was to identify changes in metabolites that may have potential to reduce the risk of CRC, in the stool samples given by the participants after consuming rice bran, as well as to understand the differences in stool metabolites in the intervention and control groups. The authors found that rice bran consumption led to changes in 93 metabolites, 33 of which increased, while 60 metabolites decreased after 4 weeks of consumption. Metabolic pathways affected included advanced glycation end products, steroid metabolism, primary bile acid metabolism, leucine, isoleucine and valine metabolism, methionine, cysteine, S-adenosyl methionine and taurine metabolism, inositol metabolism, vitamin B6 metabolism and benzoate metabolism. The authors hypothesise that these metabolic changes may have potential for the prevention of cancer and they should be further explored in larger studies.
Abstract
Rice bran (RB) consumption has been shown to reduce colorectal cancer (CRC) growth in mice and modify the human stool microbiome. Changes in host and microbial metabolism induced by RB consumption was hypothesised to modulate the stool metabolite profile in favour of promoting gut health and inhibiting CRC growth. The objective was to integrate gut microbial metabolite profiles and identify metabolic pathway networks for CRC chemoprevention using non-targeted metabolomics. In all, nineteen CRC survivors participated in a parallel randomised controlled dietary intervention trial that included daily consumption of study-provided foods with heat-stabilised RB (30 g/d) or no additional ingredient (control). Stool samples were collected at baseline and 4 weeks and analysed using GC-MS and ultra-performance liquid chromatography-MS. Stool metabolomics revealed 93 significantly different metabolites in individuals consuming RB. A 264-fold increase in β-hydroxyisovaleroylcarnitine and 18-fold increase in β-hydroxyisovalerate exemplified changes in leucine, isoleucine and valine metabolism in the RB group. A total of thirty-nine stool metabolites were significantly different between RB and control groups, including increased hesperidin (28-fold) and narirutin (14-fold). Metabolic pathways impacted in the RB group over time included advanced glycation end products, steroids and bile acids. Fatty acid, leucine/valine and vitamin B6 metabolic pathways were increased in RB compared with control. There were 453 metabolites identified in the RB food metabolome, thirty-nine of which were identified in stool from RB consumers. RB consumption favourably modulated the stool metabolome of CRC survivors and these findings suggest the need for continued dietary CRC chemoprevention efforts.
Methodological quality
Jadad score
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2
Allocation concealment
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Not applicable
