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

• Published in: The Journal of nutrition Vol. 134; no. 3; pp. 493 - 500
• Main Authors: Moreau, Noëlle M., Champ, Martine M., Goupry, Stéphane M., Le Bizec, Bruno J., Krempf, Michel, Nguyen, Patrick G., Dumon, Henri J., Martin, Lucile J.
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Elsevier Inc 01.03.2004; American Society for Nutritional Sciences; American Institute of Nutrition; American Society for Nutrition
• Subjects: Acute Disease; Animals; Biological and medical sciences; Bowel disease; butyrate; Butyrates - metabolism; Carbohydrates; Carbon Dioxide - blood; Carbon Isotopes; Cecum - metabolism; Chronic Disease; colitis; Colitis - chemically induced; Colitis - metabolism; Colon - metabolism; Dextran Sulfate - pharmacology; Digestion - physiology; Drinking Behavior; Feeding Behavior; Feeding. Feeding behavior; Food and Nutrition; Fundamental and applied biological sciences. Psychology; Gastrointestinal Transit - physiology; Intestinal Mucosa - metabolism; Isotope Labeling - methods; Ketone Bodies - metabolism; Life Sciences; Male; Metabolism; rat; Rats; Rats, Sprague-Dawley; resistant starch; Rodents; Starch - pharmacology; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Weight Gain - physiology; AA; RS; BD; colitis; butyrate; rat; DSS; RBWG; UC; C4; resistant starch; APE; metabolism; BHB; Rat; Digestive system; Rodentia; Resistant starch; Sulfates; Uptake; Butyrate; In vivo; Vertebrata; Mammalia; Animal; Digestive diseases; Intestinal disease; Oxidation; Colon; BUTYRATE; METABOLISM; COLITIS; RAT; RESISTANT STARCH
• ISSN: 0022-3166; 1541-6100
• DOI: 10.1093/jn/134.3.493

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.