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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

Postprandial hyperglycemia and insulin secretion depend on many factors, such as food composition, carbohydrate type and processing. The purpose of this study was to evaluate the effects of foods differing in composition in nonobese clinically normal dogs. These dogs were offered in a single meal one of the four foods. Blood samples were collected before feeding and during the 180 min after the meal. Plasma glucose and insulin concentrations were determined. The integrated areas under the postprandial glucose and insulin response curves were calculated. Times to response peaks, maximum plasma insulin elevation, area under the insulin response curve and the insulinemic index differed between dog foods. Crude fiber content had no significant effect. The time to glucose peak was higher and the time to insulin peak lower with the food highest in protein and ether extract content. The time to glucose peak was correlated to protein, fat and nitrogen-free extract content of foods, whereas the time to insulin peak and the area under the insulin curve were correlated to protein and nitrogen-free extract. INDEXING KEY WORDS: * dog foods * glycemic index * insulinemic index * dogs