Abstract

Increased selenium (Se) status has beneficial outcomes, including decreased colorectal cancer risk, yet obesity may interfere with Se metabolism. Commensal bacteria can influence colon carcinogenesis and Se influences the microbiome, including production of volatile fatty acids by these microbes. We sought to determine whether a poorly digestible source of Se, high‐Se wheat bran (SeBR), could target Se to the hind gut microbial community. We also tested the hypothesis that dietary methionine (MET) can compete with selenomethionine (SeMET) but not selenite (SEL) during protein synthesis, to affect the accumulation of Se in tissues relevant to obesity. Rats were fed SeBR, SeMET or SeMET + bran, and in a separate experiment rats were fed Se in varying ratios of SeMET:SEL alongside adequate or marginal levels of MET. Results show that SeBR feeding or SeMET + bran increased fecal levels of Se above SeMET feeding alone. We also found an interactive effect of SeMET:SEL ratio × Se level on total liver Se, effects of SeMET:SEL ratio and Se level on total kidney Se and a 3‐way interaction of MET level × SeMET:SEL ratio × Se level on muscle Se. This work demonstrates that Se form and diet composition can affect delivery of Se to the colon, and thus has potential to impact the hindgut microbiome. We also show that tissues important to obesity‐related co‐morbidities respond differentially to dietary Se, MET level and SeMET:SEL ratio.

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