Resistant starch modulates in vivo colonic butyrate uptake and its oxidation in rats with dextran sulfate sodium-induced colitis

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.sub.4]), a colonic cell fuel source. In the present study, we hypothesized that if inflammation is related to decreased [C.sub.4] utilization by the colonic mucosa, RS supplementation should restore [C.sub.4] use simultaneously with an increase in the amount of [C.sub.4] present in the digestive tract. Hence, we compared, in vivo, the cecocolonic uptake of [C.sub.4] and its oxidation into C[O.sub.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-.sup.13]C]-C4 (20 [micro]mol in 1 h), concentrations and [sup.13]C-enrichment of [C.sub.4], ketone bodies, and C[O.sub.2] were quantified in the abdominal aorta and portal vein. Portal blood flow was recorded. During acute colitis, [sup.13][C.sub.4] uptake and [sup.13][CO.sub.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.sub.4] uptake as BD-DSS rats in spite of higher [C.sub.4] cecocolonic disposal. After 14 d, [C.sub.4] uptake was higher in RS-DSS than in BD-DSS rats. Thus, the increased utilization of C4 by the mucosa is subsequent to evidence of healing and appears to be a consequence rather than a cause of this RS healing effect. KEY WORDS: * butyrate * metabolism * colitis * rat * resistant starch