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Biochemical and Molecular Actions of Nutrients

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

Noëlle M. Moreau^*,, Martine M. Champ^,, Stéphane M. Goupry^*,, Bruno J. Le Bizec^**, Michel Krempf, Patrick G. Nguyen^*,, Henri J. Dumon^*, and Lucile J. Martin^*,,1

^* Unité de Nutrition et d’Endocrinologie, Ecole Nationale Vétérinaire, Nantes, France; Laboratoire des Fonctions Digestives et Nutrition Humaine, Institut National de la Recherche Agronomique, Nantes, France; ^** Laboratoire d’Etudes des Résidus et des Contaminants dans les Aliments, Ecole Nationale Vétérinaire, Nantes, France; et Centre de Recherche en Nutrition Humaine, Nantes, France

¹To whom correspondence should be addressed. E-mail: lucile.martin{at}vet-nantes.fr.

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 (C₄), a colonic cell fuel source. In the present study, we hypothesized that if inflammation is related to decreased C₄ utilization by the colonic mucosa, RS supplementation should restore C₄ use simultaneously with an increase in the amount of C₄ present in the digestive tract. Hence, we compared, in vivo, the cecocolonic uptake of C₄ and its oxidation into CO₂ 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 [1-¹³C]-C₄ (20 µmol in 1 h), concentrations and ¹³C-enrichment of C₄, ketone bodies, and CO₂ were quantified in the abdominal aorta and portal vein. Portal blood flow was recorded. During acute colitis, ¹³C₄ uptake and ¹³CO₂ 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 C₄ uptake as BD-DSS rats in spite of higher C₄ cecocolonic disposal. After 14 d, C₄ 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

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