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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

The incidence of childhood obesity is rising dramatically throughout industrialised countries. To evaluate and study the impact of childhood obesity on lipoprotein metabolism, we developed a new animal model of premature obesity. Yucatan mini-pigs aged 4 months were studied over a 12-month period from childhood to adulthood. Animals were divided into two groups: the first group were overfed a Western misbalanced diet; the second group were normally fed a recommended human-type diet. Cholesterol and triacylglycerol concentrations in VLDL-, LDL- and HDL-lipoproteins were followed from baseline to adulthood by fast protein liquid chromatography. At 10 (the end of sexual maturation) and 16 months old (adulthood), liver, visceral and subcutaneous adipose tissues were sampled. Real-time RT-PCR was performed in order to compare apo AI, apo B, apo C-III, PPAR-??, insulin receptor and lipoprotein lipase gene expression between groups and ages. Differences between groups were observed only after sexual maturity. Adult overfed mini-pigs had a higher LDL-cholesterol:HDL-cholesterol ratio (P<0??05; 0??55 (SE 0??06) for overfed v. 0??42 (SE 0??04) for normally fed pigs at the tenth month of the study). In both groups, VLDL-triacylglycerol decreased (P<0??05). VLDL-triacylglycerol evolution in the overfed group was associated with an increase in LDL-triacylglycerol plasma concentrations (P<0??05) after sexual maturation. LDL-triacylglycerol concentration in overfed mini-pigs went from an average of 0??28 mmol/l before sexual maturation to reach an average concentration of 0??56 mmol/l afterwards. This phenomenon has never been observed in similar studies when obesity is induced in adult mini-pigs and may represent a specific hallmark of an obesity induced during sexual maturity. [ABSTRACT FROM PUBLISHER]