Resistant Starch Modulates In Vivo Colonic Butyrate Uptake and Its Oxidation in Rats with Dextran Sulfate Sodium-Induced Colitis

Abstract

We previously demonstrated improvements of colonic lesions due to dextran sulfate sodium (DSS) in rats after 7 d of supplementation with resistant starch (RS) type 3, a substrate yielding high levels of butyrate (C(4)), a colonic cell fuel source. In the present study, we hypothesized that if inflammation is related to decreased C(4) utilization by the colonic mucosa, RS supplementation should restore C(4) use simultaneously with an increase in the amount of C(4) present in the digestive tract. Hence, we compared, in vivo, the cecocolonic uptake of C(4) and its oxidation into CO(2) and ketone bodies in control and DSS-treated rats fed a fiber-free basal diet (BD) or a RS-supplemented diet. Sprague-Dawley rats (n = 60) were used. DSS treatment was performed to induce acute colitis and then to maintain chronic colitis. After cecal infusion of [1-(13)C]-C(4) (20 micro mol in 1 h), concentrations and (13)C-enrichment of C(4), ketone bodies, and CO(2) were quantified in the abdominal aorta and portal vein. Portal blood flow was recorded. During acute colitis, (13)C(4) uptake and (13)CO(2) production were lower in DSS rats than in controls. During chronic colitis, DSS rats did not differ from controls. After 7 d of chronic colitis, RS-DSS rats exhibited the same C(4) uptake as BD-DSS rats in spite of higher C(4) cecocolonic disposal. After 14 d, C(4) uptake was higher in RS-DSS than in BD-DSS rats. Thus, the increased utilization of C(4) by the mucosa is subsequent to evidence of healing and appears to be a consequence rather than a cause of this RS healing effect.

Interactive Effects of Dietary Resistant Starch and Fish Oil on Short-Chain Fatty Acid Production and Agonist-Induced Contractility in Ileum of Young Rats

“…This adds to the well-documented effects of n-3 PUFA in cardiovascular disease and prevention of sudden cardiac death (44) and for bowel cancer prevention (45) in older populations. The role that n-3 PUFA and SCFA, especially butyrate, play in the developing bowel and later prevention of disease is also being recognized (4,(46)(47)(48)(49). The mechanisms whereby specific nutrients such as n-3 PUFA, antioxidants, and butyrate ameliorate gut inflammatory conditions, where contractility is known to be compromised, are being elucidated by in vitro studies.…”

From the gut to the peripheral tissues: the multiple effects of butyrate

“…In healthy rats fed a fibre-free or a RS-enriched diet and using [1-13 C]butyrate intra-caecal perfusion, the flux of butyrate production was 0·7-1·8 mmol/min whereas portal flux was from 0·2 to 0·4 mmol/min and parietal utilisation from 0·9 to 1·8 mmol/min (87) . In unfed pigs with an intracaecal perfusion of [1][2][3][4][5][6][7][8][9][10][11][12][13] ]C-butyrate, the parietal utilisation of butyrate varied from 60 to 120 mmol/min when the concentration of perfused [1][2][3][4][5][6][7][8][9][10][11][12][13] ]C-butyrate varied from 0 to 160 mmol/min (L Martin, unpublished results).…”

The Effect of Microbiota and the Immune System on the Development and Organization of the Enteric Nervous System

“…Resistant starch diet (RSD), which enhances luminal SCFA concentration, 52 specifically increased the proportion of excitatory cholinergic neurons in the colon, but had no effect on nNOS + neurons, resulting in decreased colonic transit time. Intrarectal administration of butyrate, but not acetate or propionate, mimicked the effect of RSD.…”