The effect of L-rhamnose on gastrointestinal transit rates, short chain fatty acids and appetite regulation

Abstract

It has been hypothesised that the appetite‐suppressing effects associated with the consumption of non‐digestible carbohydrates (NDC) could be attributed to their effect on intestinal transit rates as well as the production of short chain fatty acids (SCFA) following their microbial fermentation(1). An acute elevation in colonic production of the SCFA propionate has previously been shown to reduce ad libitum energy intake and to increase plasma concentrations of the anorexigenic gut hormones glucagon‐like peptide‐1 (GLP‐1) and peptide YY (PYY) in humans acutely(2). The aim of conducting this pilot study was to determine the effects of the consumption of L‐rhamnose, a reportedly propionate‐producing compound(3), on gut transit times. We hypothesised that L‐rhamnose would increase plasma propionate leading to a reduction in appetite, independent of changes in gastrointestinal transit times. We used a dual13C octanoic acid/lactose13C‐ureide breath test to measure intestinal transit times following the consumption of 25 g/d L‐rhamnose, compared with inulin and cellulose, in ten healthy humans in a randomised cross‐over design. In addition, breath H2 measurements, which are routinely used as a marker of colonic fermentation(4), were collected. Gastric emptying (GE) and orocaecal transit times (OCTT) were derived from the breath13C data and compared with breath H2 excretion times. In addition, plasma SCFA and PYY concentrations were measured and visual analogue scales were completed by participants. Areas under the curve (AUC) were calculated using the trapezoidal rule. Data were compared between groups using one‐way ANOVA. Based on the13C data, L‐rhamnose significantly slowed GE rates compared to cellulose (effect size: mean ± SEM; 0.35 ± 0.13 h, P = 0.023) and inulin (0.30 ± 0.11 h, P = 0.023) but there was no difference in OCTT between treatments (P = 0.21). OCTT measured from breath13C data was highly correlated with breath H2 for inulin (r2 = 0.89, P < 0.001) but not for L‐rhamnose or cellulose (P = 0.63‐0.77). The breath H2 data suggested fermentation of L‐rhamnose occurred before it reached the caecum. L‐rhamnose consumption significantly increased the AUC0‐480 for plasma propionate versus cellulose (effect size: 1.36 ± 0.15 μM x min, P < 0.001) and inulin (effect size: 1.41 ± 0.13 μM x min, P < 0.001) as well as the AUC0‐480 for plasma PYY versus cellulose (effect size: 9.77 ± 4.0 pmol/L x min, P = 0.037) and inulin (effect size: 16.41 ± 4.16 pmol/L x min, P = 0.003). There was no difference in subjective appetite measures between groups (P = 0.37). In conclusion, the NDCs tested had a minimal effect on intestinal transit time. Our data suggest that L‐rhamnose is partially fermented in the small intestine, despite L‐rhamnose previously being considered to reach the colon intact, and that breath H2 reflects the site of gastrointestinal fermentation and is only a reliable marker of OCTT for certain NDCs (e.g. inulin). Future studies should focus on investigating the appetite‐suppressing potential of L‐rhamnose.